DETAILED NOTES ON NEUROLOGICAL NURSING KMTC.pptx

NEUROLOGICAL NURSING

NEUROLOGIC ASSESSMENT

HEALTH HISTORY An important aspect of the neurologic assessment is the history of the present illness. Observing overall appearance, mental status, posture, movement and affect. Details about the onset, character, severity, location, duration, and frequency of symptoms and signs; associated complaints; precipitating, aggravating, and relieving factors; progression, remission, and exacerbation; and the presence or absence of similar symptoms among family members

Enquire about any family history of genetic diseases Included in the health history is a review of the medical history, including a system-by-system evaluation. Enquire about any history of trauma or falls that may have involved the head or spinal cord. Questions regarding the use of alcohol, medications, and recreational drugs are also asked .

PHYSICAL EXAMINATION There are 12 pairs of cranial nerves originating from nuclei in the inferior surface of the brain, some sensory, some motor and some mixed. Their names and numbers are:

12 Pairs of Cranial Nerves I. Olfactory: sensory II. Optic: sensory III. Oculomotor: motor IV. Trochlear: motor V. Trigeminal: mixed VI. Abducent: motor VII. Facial: mixed VIII. Vestibulocochlear (auditory): sensory IX. Glossopharyngeal: mixed X. Vagus: mixed XI Accessory: motor XII. Hypoglossal: motor

CRANIAL NERVES EXAMINATION I: Olfactory nerve Function : Sense of smell Evaluation: Smell is tested in each nostril separately by placing stimuli under one nostril and occluding the opposing nostril. The stimuli used should be non-irritating and identifiable. Some example stimuli include cinnamon, cloves, and toothpaste. Bilateral loss can occur with rhinitis, smoking or aging. Unilateral loss indicates a possible nerve lesion or deviated septum.

II: Optic nerve Function: Visual fields and acuity Evaluation: Visual fields are assessed by asking the patient to cover one eye while the examiner tests the opposite eye. The examiner wiggles the finger in each of the four quadrants and asks the patient to state when the finger is seen in the periphery. The examiner's visual fields should be normal, since it is used as the baseline. Visual acuity is tested in each eye separately. Ensure the patient's vision is corrected with eyeglasses or a pinhole. The patient is asked to read progressively smaller lines on the near card or Snellen chart . Fundoscopy

III, IV, VI: Oculomotor nerve, Trochlear nerve, Abducens nerve Function: Ocular and extraocular movements, pupillary response

Evaluation : Eye movements are tested by standing one meter in front of the patient and asking the patient to follow a target with eyes only, and not the head. The target is moved in an "H" shape and the patient is asked to report any diplopia. Then, the target is held at the lateral ends of the patient's visual field.

Nystagmus is tested for. One or two beats is a normal finding. The accommodation reflex is tested by moving the target towards the patient's nose. As the eyes converge, the pupils should constrict. The optokinetic nystagmus test is optional and involves asking the patient to look at a strip of vertical lines moving horizontally across visual field. Nystagmus is normally observed.

Extraocular movements are tested by inspecting for ptosis, eye position and nystagmus. The pupil size is measured, its shape and any asymmetry is tested. A commonly used abbreviation to describe normal pupils is PERRLA (pupils equal, round and reactive to light and accommodation).

Pupillary light reflex is tested by having the patient stare into the distance as the examiner shines the penlight obliquely into each pupil. Pupillary constriction is tested for on the eye examined (direct response) and on the opposite eye (consensual response).

The swinging flashlight test involves moving the light between the two pupils. Normally both direct and consensual responses are elicited when the light shines on an eye, and some dilation will occur during the swing between.

V:Trigeminal nerve Function : Facial Sensation Evaluation: Light touch is tested in each of the three divisions of the trigeminal nerve and on each side of the face using a cotton wisp or tissue paper. The ophthalmic division is tested by touching the forehead, the maxillary division is tested by touching the cheeks, and the mandibular division is tested by touching the chin. Be careful not to test the mandibular division too laterally, as the mandible is innervated by the great auricular nerve .

A common mistake is to use a stroking motion, which will trigger pain and temperature nerves. Instead, a point stimulus should be applied. For pain and temperature repeat the same steps as light touch but use a sharp object and a cold tuning fork respectively. Corneal reflex is conducted along with the facial nerve section of the test. Note the sensory innervation of the cornea is provided by the trigeminal nerve while the motor innervation for blinking the eye is provided by the facial nerve.

Muscles of mastication (temporalis, masseter) should be inspected for atrophy. Palpate the temporalis and masseter as the patient clenches the jaw. The pterygoids can be tested by asking the patient to keep the mouth open against resistance, and move from side to side against resistance. A jaw jerk reflex can be tested by placing a finger over the patient's chin and then tapping the finger with a reflex hammer. Normally the jaw moves minimally.

VII: Facial nerve Function: Facial muscles Evaluation: Inspect for facial asymmetry and involuntary movements. Motor 1) Raise both eyebrows 2) Frown 3) Close both eyes tightly so that you can not open them. Test muscular strength by trying to open them 4) Show both upper and lower teeth 5) Smile 6) Puff out both cheeks Sensory : test for taste

VIII: Vestibulocochlear Function: Hearing Evaluation: Hearing is tested by whispering numbers in one ear as patient covers the other and ask the patient to repeat the numbers. Alternatively, have patient close their eyes and say "left" or "right" depending on the side from which they hear the sound. Vigorously rub fingers together in one ear at a time to produce rustling sound. Conduct the Rinne test and Weber test. Vestibular Function

IX and X: Glossopharyngeal and Vagus Function: Taste, pharyngeal movement Evaluation: Gag response Visualizing uvula deviation away from affected side on articulating "AHH" with tongue depressor. Palatal articulation "KA" Guttural articulation "GO"

XI: Accessory nerve Function: Shoulder girdle muscles Evaluation: Shrug shoulders Turn head from side to side

XII: Hypoglossal Function : Tongue movements Evaluation: Stick out tongue and move it to one side, then the other Inspect for tongue atrophy, fasciculations or asymmetry in movement or appearance

Assignment: Read and make notes on peripheral nerves examination.

Examining the Reflexes The motor reflexes are involuntary contractions of muscles or muscle groups in response to abrupt stretching near the site of the muscle’s insertion. The tendon is struck directly with a reflex hammer.

Testing these reflexes enables the examiner to assess involuntary reflex arcs that depend on the presence of afferent stretch receptors, spinal synapses, efferent motor fibers, and a variety of modifying influences from higher levels. Common reflexes that may be tested include the deep tendon reflexes (biceps, brachio radialis , triceps, patellar, and ankle reflexes) and Superficial reflexes

Deep tendon reflexes are graded on a scale of 0 to 4: 0 No response 1+ Diminished (hypoactive) 2+ Normal 3+ Increased (may be interpreted as normal) 4+ Hyperactive ( hyperreflexia )

The major superficial reflexes include corneal, gag or swallowing, upper/lower abdominal, cremasteric (men only), plantar, and perianal. These reflexes are graded differently than the motor reflexes and are noted to be present (+) or absent (-).

Assignment: Read and make notes on reflexes and co-ordination of the neurological system.

ASSESSMENT OF LEVEL OF CONCIOUSNESS Glasgow Coma Scale The Glasgow Coma Scale ( GCS ) is a clinical scale used to reliably measure a person's level of consciousness after a brain injury.

The GCS assesses a person based on their ability to perform eye movements, speak, and move their body. These three behaviors make up the three elements of the scale: eye, verbal, and motor. A person's GCS score can range from 3 (completely unresponsive) to 15 (responsive). This score is used to guide immediate medical care after a brain injury (such as a car accident) and also to monitor hospitalized patients and track their level of consciousness

Lower GCS scores are correlated with higher risk of death. However, the GCS score alone should not be used on its own to predict the outcome for an individual person with brain injury.

Scoring The Glasgow Coma Scale is used for people above the age of two and composed of three tests: eye, verbal, and motor responses.

The Glasgow Coma Scale is reported as the combined score (which ranges from 3 to 15) and the score of each test (E for eye, V for Verbal, and M for Motor). For each test, the value should be based on the best response that the person being examined can provide

Eye response (E) There are four grades starting with the most severe: No opening of the eye Eye opening in response to pain stimulus. A peripheral pain stimulus, such as squeezing the lunula area of the person's fingernail is more effective than a central stimulus such as a trapezius squeeze, due to a grimacing effect. Eye opening to speech. Not to be confused with the awakening of a sleeping person; such people receive a score of 4. Eyes opening spontaneously NT (Not testable). Examples for this would include severe damage to the eyes, sedation from drugs, and paralysis.

Verbal response (V) There are five grades starting with the most severe: No verbal response Incomprehensible sounds. Moaning but no words. Inappropriate words. Random or exclamatory articulated speech, but no conversational exchange. Speaks words but no sentences. Confused. The person responds to questions coherently but there is some disorientation and confusion. Oriented. Person responds coherently and appropriately to questions such as the person’s name and age, where they are and why, the year, month, etc. NT (Not testable). Examples for this would include intubation, deafness, language barrier, sedation from drugs, and paralysis.

Motor response (M) There are six grades starting with the most severe: No motor response. Lack of any motor response should raise suspicion for spinal cord injury. Abnormal Extension in response to pain. Different guidelines report different evaluation of abnormal extension. While some sources indicate extension at the elbow is sufficient,other sources use the language " decerebrate posturing". It is important to note that the original publication of the Glasgow Coma Scale explicitly avoided the term " decerebrate extension" because it implied specific anatomical findings.

Abnormal Flexion in response to pain. Different guidelines report different evaluation. While some sources focus on arm movements, other sources use the term "decorticate posturing". Normal Flexion (absence of abnormal posturing; unable to lift hand past chin with supraorbital pain but does pull away when nailbed is pinched) Localizes to pain (purposeful movements towards painful stimuli; e.g., brings hand up beyond chin when supraorbital pressure applied) Obeys commands (the person does simple things as asked) NT (Not testable). Examples for this would include spinal cord injury, sedation from drugs, and paralysis.

Eye opening response Spontaneous 4 To voice 3 To pain 2 None 1 Verbal response Oriented 5 Confused 4 Inappropriate words 3 Incomprehensible sounds 2 None 1

Best motor response Obeys command 6 Localizes pain 5 Withdraws 4 Flexion 3 Extension 2 No response 1 If the patient is comatose, with localized signs such as abnormal pupillary and motor responses, it is assumed that neurologic disease is present until proven otherwise.

If the patient is comatose and pupillary light reflexes are preserved, a toxic or metabolic disorder is suspected.

Read and make notes on the pediatric scoring using the Glasgow coma scale.

AVPU SCALE Description: AVPU scale ( Alert, Voice, Pain, Unresponsive ) is a system, which is taught to healthcare professionals and first aiders on how to measure and record the patient's level of consciousness. It is a mplification of the GCS Scale which assesses a patient's response using Eyes, Voice and Motor skills as measures. The AVPU has only one of four possible outcomes: 1 . Alert Patient is fully awake (though not necessarily orientated), will have spontaneously open eyes, and will respond to voice (thought may be confused). They will have bodily motor function. 3

. 2. Voice The patient makes some sort of response when you talk to them. This could be through the eyes, which open when you speak to them, or by voice which may only be as little as a grunt. Or, it could be by moving a limb when prompted to do so by the rescuer. 3.Pain A patient may respond by using any of the three components when pain stimulus is used on them (Eyes, Voice, Movementl . A fully conscious patient will locate the pain and push it away, whereas a patient who is not alert and not responded to voice may only manifest involuntary flexion or extension of a limb. 4. Unresponsive This outcome is noted if the patient does not give any Eye, Voice or Motor response

ACDU It is a four point scale that has been suggested by others and was a tool chosen to assess against AVPU. When preference was expressed the nurses liked ACDU. It refers to alert,confused, drowsy and unresponsive

ACUTE CONDITIONS

SPACE OCCUPYING LESIONS

PRIMARY BRAIN TUMORS A brain tumor is a localized intracranial lesion that occupies space within the skull. Tumors usually grow as a spherical mass, but they can grow diffusely and inﬁltrate tissue. The effects of neo- plasms occur from the compression and inﬁltration of tissue.

A variety of physiologic changes result, causing any or all of the following pathophysiologic events: • Increased intracranial pressure (ICP) and cerebral edema • Seizure activity and focal neurologic signs • Hydrocephalus • Altered pituitary function

Primary brain tumors originate from cells and structures within the brain. Secondary, or metastatic, brain tumors develop from structures outside the brain and occur in 20% to 40% of all patients with cancer.

The cause of primary brain tumors is unknown. The only known risk factor is exposure to ionizing radiation. Additional possible causes included use of cellular telephones Exposure to high-tension wires, use of hair dyes, head trauma, dietary exposure to such factors as nitrates

Pathophysiology Brain tumors may be classiﬁed into several groups: those arising from the coverings of the brain (e.g. dural meningioma), Those developing in or on the cranial nerves ( eg , acoustic neuroma), Those originating within brain tissue (e.g. gliomas), and metastatic lesions originating elsewhere in the body. Tumors of the pituitary and pineal glands and of cerebral blood vessels are also types of brain tumors.

GLIOMA Glial tumors, the most common type of brain neoplasm, are divided into many categories. Astrocytoma s are the most common type of glioma and are graded from I to IV, indicating the degree of malignancy. Glioblastoma multiforme (astrocytoma grades III and IV) Oligodendrocytoma (low and high grades) Ependymoma (grades I to IV) . Medulloblastoma

MENINGIOMAS Meningiomas , which represent 20% of all primary brain tumors, are common benign encapsulated tumors of arachnoid cells on the meninges ). They are slow-growing and occur most often in middle-aged adults (more often in women).. Standard treatment is surgery with complete removal or partial dissection

ACOUSTIC NEUROMAS An acoustic neuroma is a tumor of the eighth cranial nerve, the cranial nerve most responsible for hearing and balance. It usually arises just within the internal auditory meatus , where it frequently expands before ﬁlling the cerebellopontine recess. The patient usually experiences loss of hearing, tinnitus, and episodes of vertigo and staggering gait. As the tumor becomes larger, painful sensations of the face may occur on the same side as a result of the tumor’s compression of the ﬁfth cranial nerve.

ANGIOMAS: These are masses composed largely of abnormal blood vessels. Are found either in or on the surface of the brain

Clinical Manifestations Brain tumors can produce either focal or generalized neurologic signs and symptoms. Generalized symptoms reflect increased ICP,i.e headache, nausea and vomiting, and a sixth-nerve palsy and the most common focal or specific signs and symptoms result from tumors interfering with functions in specific brain regions.

LOCALIZED SYMPTOMS Hemiparesis Seizures, Mental status changes Visual alterations, Alterations in cognition, and language disturbances such as aphasia(A comprehension and communication (reading, speaking, or writing) disorder resulting from damage or injury to the specific area in the brain).

Assessment and Diagnostic Findings The history of the illness and the manner and time frame in which the symptoms evolved are key components in the diagnosis of brain tumors.

A neurologic examination indicates the areas of the CNS involved. Computed tomography (CT) scans gives specific information concerning the number, size, and density of the lesions. MRI also helps in diagnosis. Cerebral angiography provides visualization of cerebral blood vessels and can localize most cerebral tumors. An electroencephalogram (EEG) can detect an abnormal brain wave in regions occupied by a tumor and is used to evaluate temporal lobe seizures

Medical Management A variety of medical treatment modalities, including chemotherapy and external-beam radiation therapy , are used alone or in combination with surgical resection . Radiation therapy, the cornerstone of treatment of many brain tumors, decreases the incidence of recurrence of incompletely resected tumors. Corticosteroids may be used before and after treatment to reduce cerebral edema and promote a smoother, more rapid recovery.

SURGICAL MANAGEMENT: The objective of surgical management is to remove or destroy the entire tumor without increasing the neurologic deficit (paralysis, blindness) or to relieve symptoms by partial removal (decompression). Nursing Management The patient with a brain tumor may be at an increased risk for aspiration due to cranial nerve dysfunction. Preoperatively, the gag reflex and ability to swallow are evaluated.

In patients with diminished gag response, care includes teaching the patient to direct food and fluids toward the unaffected side, having the patient sit upright to eat, offering a semisoft diet, and having suction readily available. The nurse performs neurologic checks, monitors vital signs, maintains a neurologic flow chart, spaces nursing interventions to prevent rapid increase in ICP, and reorients the patient when necessary to person, time, and place.

Patients with changes in cognition caused by the lesion require frequent reorientation. Motor function is checked at intervals because specific motor deficits may occur, depending on the tumor’s location. Sensory disturbances are assessed. Speech is evaluated. Eye movement and pupillary size and reaction may be affected by cranial nerve involvement.

CEREBRAL METASTASES A significant number of patients with cancer experience neurologic deficits caused by metastasis to the brain. Neurologic signs and symptoms include headache, gait disturbances, visual impairment, personality changes, altered mentation (memory loss and confusion), focal weakness, paralysis,aphasia , and seizures.

Medical Management The treatment of metastatic brain cancer is palliative and involves eliminating or reducing serious symptoms. The therapeutic approach includes radiation therapy , surgery (usually for a single intracranial metastasis), and chemotherapy. More often some combination of these treatments is the optimal method. PHARMACOLOGIC THERAPY Corticosteroids are useful in relieving headache and alterations in level of consciousness.

It is thought that corticosteroids ( dexamethasone , prednisone) reduce inflammation around the metastatic deposits and decrease the edema surrounding them. Other medications used include osmotic agents (mannitol) to decrease the fluid content of the brain. Antiseizure agents (e.g. phenytoin) are used to prevent and treat seizures.

Venous thromboembolic events, such as deep vein thrombosis (DVT) and pulmonary embolism (PE), occur in about 15% of patients and are associated with significant morbidity. If the patient has severe pain, morphine can be infused into the epidural or subarachnoid space through a spinal needle and a catheter as near as possible to the spinal segment where the pain is projected.

VASCULAR DISORDERS

Assignment: Read and make notes on transient ischemic attack.

CEREBROVASCULAR ACCIDENT It is also known as stroke Occurs when the supply of blood to the brain is reduced or blocked completely, which prevents brain tissue from getting oxygen and nutrients.

Cerebrovascular disorders (CVA) is an umbrella term that refers to any functional abnormality of the central nervous system (CNS) that occurs when the normal blood supply to the brain is disrupted A stroke is a medical emergency, and prompt treatment is crucial. Early action can reduce brain damage and other complications.

CVA can be divided into two major categories: Ischemic stroke ; accounts for 85% of all CVA cases. There is vascular occlusion and significant hypo perfusion of the brain tissue. Hemorrhagic stroke ; accounts for 15% of all CVA cases. There is extravasation of blood into the brain tissue or subarachnoid space .

Ischemic Stroke It refers to a sudden loss of function of the brain tissue resulting from disruption of the blood supply to a part of the brain. This event is usually the result of long-standing cerebrovascular disease .

AETIOLOGY The cause of ischemic stroke is mainly formation of a thrombus in the blood vessels occluding the blood flow to the brain. Based on the cause, ischemic stroke can be subdivided into 5 categories: Large artery thrombotic stroke: They are due to atherosclerotic plaques in the large blood vessels of the brain leading to ischemia and infarction. Small penetrating artery thrombosis; affect one or more vessels and are the most common type of ischemic stroke.

3. Cardiogenic embolic; They are associated with cardiac dysrhythmias , usually atrial fibrillation. Emboli originate from the heart and circulate to the cerebral vasculature, most commonly the left middle cerebral artery, resulting in a stroke. The last two classifications of ischemic strokes are 4. Cryptogenic strokes, which have no known cause, and 5. other strokes, from causes such as cocaine use, coagulopathies , migraine etc.

Pathophysiology In an ischemic brain attack, there is disruption of the cerebral blood flow due to obstruction of a blood vessel. This disruption in blood flow initiates a complex series of cellular metabolic events referred to as the ischemic cascade . The ischemic cascade begins when cerebral blood flow falls to less than 25 mL /100 g/min. At this point, neurons can no longer maintain aerobic respiration.

The mitochondria must then switch to anaerobic respiration, which generates large amounts of lactic acid, causing a change in the pH level. This switch to the less efficient anaerobic respiration also renders the neuron incapable of producing sufficient energy needed for cell metabolism and finally the cell ceases to function . If there is no intervention,the brain cells die leading to brain infarction.

Clinical Manifestations Numbness or weakness of the face, arm, or leg, especially on one side of the body • Confusion or change in mental status • Trouble speaking or understanding speech • Visual disturbances • Difficulty walking, dizziness, or loss of balance or coordination Loss of consiousness or seizures • Sudden severe headache There is loss of cognitive,visual,cranial nerves,motor and sensory functioning.

Visual Field Deficits Hemianopsia (loss of half of the visual field) Loss of peripheral vision Diplopia Motor Deficit Hemiplegia Ataxia Dysphagia

Sensory Deficits Paresthesia (occurs on the side opposite the lesion) Verbal Deficits Expressive aphasia(is a form of aphasia in which the person knows what they want to say but is unable to produce the words or sentence). Receptive aphasia(is a language disorder that makes it hard for a person to understand spoken or written language). Cognitive Deficits Short- and long-term memory loss Decreased attention span Impaired ability to concentrate Poor abstract reasoning Altered judgment

Emotional Deficits Loss of self-control Emotional instability Decreased tolerance to stressful situations Depression Withdrawal Fear, hostility, and anger Feelings of isolation

RISK FACTORS non-modifiable Advanced age- elderly, gender- men more affected race – african americans Modifiable Hypertension diabetes cardiovascular disease- high cholesterol, obesity High red cell count

Oral contraceptive use (increases risk, especially with coexisting hypertension, smoking, and high estrogen levels) Smoking Drug abuse (especially cocaine) Excessive alcohol consumption Cardiac structural abnormalities

Assessment and Diagnostic Findings Complete history taking physical and neurologic examination. Initial assessment focuses on airway patency, respiratory function and cardiovascular Status. Diagnostic tests such as CT scan to determine if stroke is ischemic or hemorrhagic. Other tests include ECG,Cerebral angiography and transcranial doppler studies. PET, MRI with diffusion-weighted images to localize ischemic damage

MEDICAL MANAGEMENT Clot busting medicines( thrombolytics or fibronolytics ) Platelet-inhibiting medications (aspirin, dipyridamole , clopidogrel and ticlopidine decrease the incidence of cerebral infarction in patients who have experienced CVA from suspected embolic or thrombotic causes. Use of Thrombolytic therapy; Recombinant tissue plasminogen activator( t-PA) is a genetically engineered form of t-PA, a thrombolytic substance made naturally by the body. It works by binding to fibrin and converting plasminogen to plasmin , which stimulates fibrinolysis of the atherosclerotic lesion. The patient is weighed to determine the dose of t-PA.

The minimum dose is 0.9 mg/kg; the maximum dose is 90 mg. The patient is admitted to the intensive care unit, where continuous cardiac monitoring is implemented. Vital signs are obtained every 15 minutes for the first 2 hours, every 30 minutes for the next 6 hours, then every hour for 16 hours. Airway management is instituted based on the patient’s clinical condition and arterial blood gas values.

THERAPY FOR PATIENTS WITH ISCHEMIC STROKE NOT RECEIVING t-PA Anticoagulant administration (IV heparin or low- molecularweight heparin) for ischemic strokes and careful maintenance of cerebral hemodynamics to maintain cerebral perfusion is done. Measures to reduce ICP, such as administering an osmotic diuretic ( eg , mannitol), maintaining PaCO2 within the normal range.

Other treatment measures include: Elevation of the head of the bed to promote venous drainage and to lower increased ICP Intubation with an endotracheal tube to establish a patent airway, if necessary. Continuous hemodynamic monitoring. Systolic pressure should be maintained at less than 180 mm Hg, diastolic pressure at less than 100 mm Hg. Continuous neurologic assessment to determine whether the stroke is evolving or whether other acute complications are developing, such as bleeding from anticoagulants medication. Craniotomy-brain surgery done to remove blood clot, relieve pressure or repair bleeding in the brain.

NURSING DIAGNOSIS Impaired physical mobility related to hemiparesis, loss of balance and coordination, spasticity, and brain injury Self-care deficit (hygiene, toileting, grooming, and feeding) related to stroke sequelae Disturbed sensory perception related to altered sensory reception, transmission, and/or integration Incontinence related to flaccid bladder, confusion, or difficulty in communicating.

Hemorrhagic Stroke Hemorrhagic strokes account for 15% of cerebrovascular disorders and are primarily caused by an intracranial or subarachnoid hemorrhage. Hemorrhagic strokes are caused by bleeding into the brain tissue,the ventricles, or the subarachnoid space .

Leakage of blood from a blood vessel and hemorrhage into brain tissue, causing edema, compression of brain tissue, and spasm of adjacent blood vessels. May occur outside the dura ( extradural ), beneath the dura mater (subdural), in the subarachnoid space (SAS or subarachnoid), or within the brain substance ( intracerebral ).

causes Primary intracerebral hemorrhage from a spontaneous rupture of small vessels accounts for approximately 80% of hemorrhagic strokes and is primarily caused by uncontrolled hypertension . Secondary intracerebral hemorrhage is associated with Congenital weakening of blood vessel wall with aneurysm or arteriovenous malformation (AVM). Head trauma causing dissection or rupture or vessel certain medications ( eg , anticoagulants and amphetamines)

pathophysiology Pathophysiology The pathophysiology of hemorrhagic stroke depends on the cause and type of cerebrovascular disorder. Symptoms are produced when an aneurysm or AVM enlarges and presses on nearby cranial nerves or brain tissue or, more dramatically, when an aneurysm or AVM ruptures, causing subarachnoid hemorrhage (hemorrhage into the cranial subarachnoid space). Normal brain metabolism is disrupted by the brain being exposed to blood; by an increase in ICP resulting from the sudden entry of blood into the subarachnoid space, which compresses and injures brain tissue; or by secondary ischemia of the brain resulting from the reduced perfusion pressure and vasospasm that frequently accompany subarachnoid hemorrhage.

Prevention Primary prevention of hemorrhagic stroke is the best approach. Control of hypertension, especially in individuals over 55 years of age, clearly reduces the risk for hemorrhagic Stroke risk screenings provide an ideal opportunity to lower hemorrhagic stroke risk by identifying high-risk individuals or groups and educating the patients and the community about recognition and prevention.

Medical Management The goals of medical treatment of hemorrhagic stroke are to allow the brain to recover from the initial insult (bleeding), to prevent or minimize the risk for rebleeding, and to prevent or treat complications. Management consists of bed rest with sedation to prevent agitation and stress, management of vasospasm, and surgical or medical treatment to prevent rebleeding. Analgesics (codeine, acetaminophen) may be prescribed for head and neck pain. The patient is ﬁtted with elastic compression stockings to prevent deep vein thrombosis, a threat to any patient on bed rest.

SURGICAL MANAGEMENT Many patients with a primary intracerebral hemorrhage are not treated surgically. However, surgical evacuation is strongly recommended for the patient with a cerebellar hemorrhage if the diameter exceeds 3 cm and the Glasgow Coma Scale score is below Surgical evacuation is most frequently accomplished via a craniotomy The patient with an intracranial aneurysm is prepared for surgical intervention as soon as the condition is considered stable. . Morbidity and mortality from surgery are high if the patient is stuporous or comatose (grade IV or V). Surgical treatment of the patient with an unruptured aneurysm is an option . The goal of surgery is to prevent bleeding in an unruptured aneurysm and further bleeding in an already ruptured aneurysm. This objective is accomplished by isolating the aneurysm from its circulation or by strengthening the arterial wall

POTENTIAL COMPLICATIONS Rebleeding Cerebral Hypoxia and Decreased Blood Flow Cerebral vasospasm resulting in cerebral ischemia; Acute hydrocephalus Seizures

INTRACRANIAL (CEREBRAL) ANEURYSM: An intracranial (cerebral) aneurysm is a dilation of the walls of a cerebral artery that develops as a result of weakness in the arterial wall. It can rupture or leak causing life threatening bleeding The cause of aneurysms is unknown, although research is ongoing. An aneurysm may be due to atherosclerosis, resulting in a defect in the vessel wall with subsequent weakness of the wall congenital defect of the vessel wall hypertensive vascular disease, head trauma advancing age

Clinical Manifestations Many of the same motor, sensory, cranial nerve, cognitive, and other functions that are disrupted following ischemic stroke are altered following a hemorrhagic stroke. In addition to that, Rupture of an aneurysm or AVM ( arteriovenous malformation) usually produces a sudden, unusually severe headache and often loss of consciousness for a variable period. There may be pain and rigidity of the back of the neck ( nuchal rigidity) and spine due to meningeal irritation.

Visual disturbances (visual loss, diplopia , ptosis ) occur when the aneurysm is adjacent to the occulomotor nerve. Tinnitus, dizziness, and hemiparesis may also occur.

SURGICAL MANAGEMENT The goal of surgery is to prevent bleeding in an unruptured aneurysm and further bleeding in an already ruptured aneurysm. This objective is accomplished by isolating the aneurysm from its circulation or by strengthening the arterial wall.

NURSING PROCESS: A complete neurologic assessment is performed initially and should include evaluation for the following: • Altered level of consciousness • Sluggish pupillary reaction • Motor and sensory dysfunction

Cranial nerve deficits ( extraocular eye movements, facial droop, presence of ptosis) • Speech difficulties and visual disturbance • Headache and nuchal rigidity or other neurologic deficits

NURSING DIAGNOSES Ineffective cerebral tissue perfusion related to bleeding. Disturbed sensory perception related to medically imposed restrictions (aneurysm precautions) Anxiety related to illness and/or medically imposed restrictions (aneurysm precautions)

Aneurysm Precautions The patient is placed on immediate and absolute bed rest in a quiet, non stressful environment because activity, pain, and anxiety elevate the blood pressure, which increases the risk for bleeding. The head of the bed is elevated 15 to 30 degrees to promote venous drainage and decrease ICP.

Thigh-high elastic compression stockings are prescribed to decrease the incidence of deep vein thrombosis resulting from immobility. The nurse administers all personal care. The patient is fed and bathed to prevent any exertion that might raise the blood pressure.

INFECTIONS

MENINGITIS Meningitis is an inflammation of the fluid and meninges, the protective membranes that surround the brain and spinal cord. Meningitis is classified as aseptic or septic. In aseptic meningitis , bacteria are not the cause of the inflammation; the cause is viral,fungal , parastic or secondary to lymphoma, leukemia, or brain abscess,chemical irritation,drug allergies. Septic meningitis refers to meningitis caused by bacteria, most commonly Neisseria meningitidis, although Haemophilus influenzae and Streptococcus pneumoniae are also causative agents .

PREDISPOSING FACTORS Overcrowding Extreme of age 5&60 Tobacco use Medical conditions-Otitis media and mastoiditis, Viral upper respiratory ,infective endocarditis Immunosuppression.- hiv,dm Disruption of anatomical cns barrier- basillar skull fracture,neurosurgery,csf shunt,cochlear implants Dural defect- traumatic,surgical,congenital Skipping vaccines Malignancy Recent travel to endemic area Other risk factors- smoking,alcoholism,injectionof drug

Pathophysiology Meningeal infections generally originate in one of two ways: -through the bloodstream as a consequence of other infections, or -by direct extension, such as might occur after a traumatic injury to the facial bones, or secondary to invasive procedures.

N. meningitidis concentrates in the nasopharynx and is transmitted by secretion or aerosol contamination. Once the causative organism enters the bloodstream, it crosses the blood–brain barrier and causes an inflammatory reaction in the meninges . Independent of the causative agent, inflammation of the subarachnoid space and pia mater occurs. Since there is little room for expansion within the cranial vault, the inflammation may cause increased intracranial pressure. (CSF) flows in the subarachnoid space, where inflammatory cellular material from the affected meningeal tissue enters and accumulates in the subarachnoid space, thereby increasing the CSF cell count

Clinical Manifestations Headache and fever are frequently the initial symptoms. Fever tends to remain high throughout the course of the illness. Nuchal rigidity (stiff neck) is an early sign. Any attempts at flexion of the head are difficult because of spasms in the muscles of the neck. Forceful flexion causes severe pain. Positive Kernig’s sign: When the patient is lying with the thigh flexed on the abdomen, the leg cannot be completely extended

Positive Brudzinski’s sign: When the patient’s neck is flexed, flexion of the knees and hips is produced; when passive flexion of the lower extremity of one side is made, a similar movement is seen in the opposite extremity. Photophobia: (extreme sensitivity to light). A rash can be a striking feature of N. meningitidis infection. Disorientation and memory impairment are common early in the course of the illness Seizures and increased intracranial pressure (ICP) are also associated with meningitis

Assessment and Diagnostic Findings Lumbar puncture is the main diagnostic test to obtain CSF for culture and Gram staining to identify the causative organism.

Medical Management Early administration of an antibiotic that crosses the blood–brain barrier into the subarachnoid space in sufficient concentration to halt the multiplication of bacteria. Penicillin antibiotics ( eg , ampicillin , piperacillin ) or one of the cephalosporins ( eg , ceftriaxone sodium, cefotaxime sodium) are used. Vancomycin hydrochloride alone or in combination with rifampin may be used if resistant strains of bacteria are identified.

Dexamethasone has been shown to be beneficial as adjunct therapy in the treatment of acute bacterial meningitis. Dehydration and shock are treated with fluid volume expanders. Seizures, which may occur in the early course of the disease,are controlled with phenytoin (Dilantin). Increased ICP is treated as necessary

Nursing Management Neurologic status and vital signs are continually assessed. Pulse oximetry and arterial blood gas values are used to quickly identify the need for respiratory support as the increasing ICP compromises the brain stem. Insertion of a cuffed endotracheal tube (or tracheotomy) and mechanical ventilation may be necessary to maintain adequate tissue oxygenation Intravenous(IV) fluid replacement may be prescribed, but care is taken not to increase the ICP. Fevers are managed with antipyretics

Protecting the patient from injury secondary to seizure activity or altered level of consciousness Preventing complications associated with immobility, such as pressure ulcers and pneumonia Instituting droplet precautions until 24 hours after the initiation of antibiotic therapy An important aspect of the nurse’s role is to support the patient and to assist the family in identifying others who can be supportive to them during the crisis.

ENCEPHALITIS Encephalitis is an acute inflammatory process of the brain tissue. Herpes simplex virus (HSV) is the most common cause of acute encephalitis. May cause mild flu like symptoms i.e. fever, headache, Severe ones- confusion, and behavioral abnormalities Focal neurologic symptoms reflect the areas of cerebral inflammation and necrosis and include behavioral change, focal seizures, dysphasia, hemiparesis, and altered level of consciousness, confusion.

Types of encephalitis Primary encephalitis- occurs when virus or other agents directly infects the brain Secondary encephalitis-results from faulty immune system, reaction to an infection elsewhere in the body

DIAGNOSIS MRI,CT scan electroencephalography (EEG), and CSF examination are used to diagnose HSV encephalitis. management Acyclovir , an antiviral agent, is the medication of choice in HSV treatment. Anti-inflammatory drugs Bed rest Plenty of fluids Other causes of encephalitis are Fungal and Arthropod borne encephalitis.

Supportive therapy Breathing assistance Iv fluids Anti-inflammatory drugs Anticonvulsant drugs

Complications Coma Persistent fatigue Weakness or lack of muscle coordination Memory problems Paralysis Hearing defects

BRAIN ABSCESS A brain abscess is a collection of infectious material within the tissue of the brain. It may occur by direct invasion of the brain from intracranial trauma or surgery; by spread of infection from nearby sites, such as the sinuses, ears, and teeth. To prevent brain abscess, otitis media, mastoiditis, sinusitis,dental infections, and systemic infections should be treated promptly.

Clinical Manifestations Headache, usually worse in the morning, is the most prevailing symptom. Vomiting. Focal neurologic signs (weakness of an extremity, decreasing vision, seizures) may occur, depending on the site of the abscess. Changes in mental status, as reflected in lethargic, confused, irritable, or disoriented behavior. Fever may or may not be present.

Assessment and Diagnostic Findings A computed tomography (CT) scan is invaluable in locating the site of the abscess. A magnetic resonance imaging (MRI) scan is also useful.

Medical Management Brain abscess is treated with antimicrobial therapy and surgical incision or aspiration. Penicillin G (20 million U) and chloramphenicol (4 to 6 g/day given intravenously in divided doses) are given. Corticosteroids may be prescribed to help reduce the inflammatory cerebral edema if the patient shows evidence of an increasing neurologic deficit. Antiseizure medications (phenytoin, phenobarbital) Complete excision of the brain abscess can be done

Nursing Management Ongoing neurologic assessment alerts the nurse to changes in ICP. Patient safety is also a key nursing responsibility. Injury may result from decreased level of consciousness and falls related to motor weakness or seizures. The nurse must assess the family’s ability to express their distress at the patient’s condition, cope with the patient’s illness and deficits, and obtain support.

HEAD INJURIES Head injury is a broad classification that includes injury to the scalp, skull, or brain. It is the most common cause of death from trauma. Damage to the brain from traumatic injury takes two forms: -primary injury and - secondary injury.

Primary injury is the initial damage to the brain that results from the traumatic event. This may include contusions, lacerations, and torn blood vessels from impact , acceleration/deceleration, or foreign object penetration. Secondary injury evolves over the ensuing hours and days after the initial injury and is due primarily to brain swelling or ongoing bleeding

PATHO PHYSIOLOGY Brain suffers traumatic injury Brain swelling or bleeding increases intracranial volume Rigid cranium allows no room for expansion of contents so intracranial pressure increases Pressure on blood vessels within the brain causes blood flow to the brain to slow

Cerebral hypoxia and ischemia occur Intracranial pressure continues to rise. Brain may herniate Cerebral blood flow ceases Brain death

TYPES OF BRAIN INJURIES Concussion A cerebral concussion is a minor head injury characterised by temporary loss of neurologic function with no apparent structural damage. The jarring of the brain may be so slight as to cause only dizziness and spots before the eyes (“seeing stars”), or it may be severe enough to cause complete loss of consciousness for a few seconds.

Contusion Cerebral contusion is a more severe injury in which the brain is bruised, with possible surface hemorrhage. The patient is unconscious for more than a few seconds or minutes. Clinical signs and symptoms depend on the size of the contusion and the amount of associated cerebral edema. The patient may lie motionless, with a faint pulse, shallow respirations, and cool, pale skin. Often there is involuntary evacuation of the bowels and the bladder.

Intracranial Hemorrhage A severe form of brain injuries leading to formation of hematomas. Hematomas (collections of blood) that develop within the cranial vault are the most serious brain injuries . A hematoma may be epidural (above the dura ), subdural (below the dura ), or intracerebral (within the brain). Major symptoms are frequently delayed until the hematoma is large enough to cause distortion of the brain and increased ICP.

Brain injury cont.d Diffuse axonal injury Diffuse axonal injury involves widespread damage to axons in the cerebral hemispheres, corpus callosum, and brain stem. With rapid acceleration and deceleration of the head shearing forces causes mechanical axonal damage It can be seen in mild, moderate, or severe head trauma and results in axonal swelling and disconnection. .patient often present in coma from time of impact and survivors are usually disabled Diagnosis is made by clinical signs in conjunction with a CT scan or MRI. Recovery depends on the severity of the axonal injury.

CLINICAL MANIFESTATIONS OF HEAD INJURIES Altered level of consciousness Confusion Pupillary abnormalities (changes in shape, size, and response to light) Altered or absent gag reflex Absent corneal reflex Sudden onset of neurologic deficits

Changes in vital signs (altered respiratory pattern, hypertension, bradycardia, tachycardia, hypothermia or hyperthermia) Vision and hearing impairment Sensory dysfunction Spasticity Headache Vertigo Movement disorders Seizures

Management Initial Physical and neurologic examinations are done.gcs CT and MRI are the primary neuroimaging diagnostic tools and are useful in evaluating soft tissue injuries. Positron emission tomography (PET scan) is done to examine the brain functioning. NB : Any individual with a head injury is presumed to have a cervical spine injury until proven otherwise. From the scene of the injury, the patient is transported on a board with the head and neck maintained in alignment with the axis of the body.

Emergency care focuses on making sure the person has enough oxygen and adequate blood supply,mantaining bp and preventing any further injury to the head and neck

MEDICAL MANAGEMENT As the damaged brain swells with edema or as blood collects within the brain, a rise in ICP occurs; Review management of increased ICP. Surgery is required for evacuation of blood clots, débridement and elevation of depressed fractures of the skull, and suture of severe scalp lacerations Treatment also includes ventilatory support, Seizure prevention by administering antiseizure drugs Fluid and electrolyte maintenance, Nutritional support,

Treatment of increased intracranial pressure Surgery is required for evacuation of blood clots, debridement and elevation of depressed fractures of the skull, and suture of severe scalp lacerations. ICP is monitored closely; if increased, it is managed by maintaining adequate oxygenation, elevating the head of the bed, and maintaining normal blood volume Devices to monitor ICP and drain CSF can be inserted during surgery or at the bedside using aseptic technique. Patient should be admitted in ICU

Pain and anxiety management. Comatose patients are intubated and mechanically ventilated to ensure adequate oxygenation and protect the airway. A nasogastric tube may be inserted because reduced gastric motility and reverse peristalsis are associated with head injury, making regurgitation and aspiration common in the first few hours. Incase of brain death, the nurse may provide information to the family and get consent for potential organ donation .

NURSING PROCESS Assessment Take a health history to include the following questions: - When did the injury occur? - What caused the injury? A high-velocity missile? An object striking the head? A fall? - What was the direction and force of the blow? A complete neurological examination is done. Physical assessement Assess for the level of consciousness using a Glasgow coma scale.

NURSING DIAGNOSES Ineffective airway clearance and impaired gas exchange related to brain injury Ineffective cerebral tissue perfusion related to increased ICP. Deficient fluid volume related to decreased LOC and hormonal dysfunction Imbalanced nutrition, less than body requirements, related to metabolic changes, fluid restriction, and inadequate intake Risk for injury (self-directed and directed at others) related to seizures, disorientation, restlessness, or brain damage

Potential for impaired skin integrity related to bed rest,hemiparesis, hemiplegia, and immobility Disturbed thought processes (deficits in intellectual function, communication, memory, information processing) related to brain injury POTENTIAL COMPLICATIONS Cerebral edema and herniation Impaired oxygenation and ventilation Post- traumatic seizures.

Spinal Cord Injury Spinal cord injury (SCI) is a major health problem. SCI occurs almost four times more often in males than females. The predominant risk factors for SCI include age, gender, and alcohol and drug use. The vertebrae most frequently involved in SCI are the 5th,6th, and 7th cervical (neck), the 12th thoracic, and the 1st lumbar vertebrae These vertebrae are the most susceptible because there is a greater range of mobility in the vertebral column in these areas. SCIs can be separated into two categories: primary injuries and secondary injuries.

Pathophysiology Damage to the spinal cord ranges from transient concussion to contusion, laceration and compression of the cord substance, to complete transection of the cord (which renders the patient paralyzed below the level of injury SCIs can be separated into two categories; primary injuries and secondary injuries; Primary injuries are as a result of the initial insult/ trauma and are usually permanent Secondary injuries are usually the result of a contusion or tear injury, in which the nerve fibres begin to swell and disintegrate.

Spinal injury… Patho cont A secondary chain of events produces ischemia, hypoxia, edema and hemorrhagic lesions which in turn result in destruction of myelin and axons. These secondary reactions, believed to be the principal causes of spinal cord degeneration at the level of injury, are now thought to be reversible 4-6 hours after injury Therefore, if the cord has not suffered irreparable damage, some method of early treatment is needed to prevent partial damage and developing into a total and permanent damage

Clinical Manifestations A complete spinal cord lesion can result in paraplegia (paralysis of the lower body) or quadriplegia (paralysis of all four extremities).There is No motor or sensory function that is preserved. Incomplete spinal cord lesions are classified according to the area of spinal cord damage. central, lateral, anterior, or peripheral. another standard classification of SCI according to the degree of sensory and motor function present after injury

“Neurologic level” refers to the lowest level at which sensory and motor functions are normal. Below the neurologic level, there is total sensory and motor paralysis, loss of bladder and bowel control (usually with urinary retention and bladder distention), loss of sweating and vasomotor tone, and marked reduction of blood pressure from loss of peripheral vascular resistance.

If conscious, the patient usually complains of acute pain in the back or neck. Respiratory dysfunction is related to the level of injury. The muscles contributing to respiration are the abdominals and intercostals (T1 to T11) and the diaphragm. In high cervical cord injury, acute respiratory failure is the leading cause of death.

Assessment and Diagnostic Findings A detailed neurologic examination is performed. Diagnostic x-rays (lateral cervical spine x-rays) and CT scanning are performed initially. An MRI scan may be ordered as a further workup if a ligamentous injury is suspected

Emergency Management The immediate management of the patient at the scene of the injury is critical, because improper handling can cause further damage and loss of neurologic function. At the scene of the injury, the patient must be immobilized on a spinal (back) board or cervical immobilizing device, with head and neck in a neutral position,to prevent an incomplete injury from becoming complete. During treatment in the emergency and x-ray departments, the patient is kept on the transfer board. The patient must always be maintained in an extended position. No part of the body should be twisted or turned, nor should the patient be allowed to sit up

Management of Spinal Cord Injuries ACUTE PHASE The goals of management are to prevent further SCI and to observe for symptoms of progressive neurologic deficits. The patient is resuscitated as necessary, and oxygenation and cardiovascular stability are maintained. Administration of high-dose corticosteroids, specifically methylprednisolone , has been found to improve motor and sensory outcomes. If endotracheal intubation is necessary, extreme care is taken to avoid flexing or extending the patient’s neck, which can result in an extension of a cervical injury.

Management of SCI requires immobilization and reduction of dislocations (restoration of normal position) and stabilization of the vertebral column. Cervical fractures are reduced and the cervical spine is aligned with some form of skeletal traction, such as skeletal tongs or calipers.

Nursing management Assessment The breathing pattern, the strength of the cough , and the lungs are auscultated , because paralysis of abdominal and respiratory muscles diminishes coughing and makes it difﬁcult to clear bronchial and pharyngeal secretions. . Motor and sensory functions are assessed through careful neurologic examination.

. The lower abdomen is palpated for signs of urinary retention and over distention of the bladder. Temperature is monitored because the patient may have periods of hyperthermia as a result of alteration in temperature control due to autonomic disruption.

Nursing Interventions PROMOTING ADEQUATE BREATHING AND AIRWAY CLEARANCE Possible impending respiratory failure is detected by observing the patient, measuring vital capacity, monitoring oxygen saturation through pulse oximetry, and monitoring arterial blood gas values. Early and vigorous attention to clearing bronchial and pharyngeal secretions can prevent retention of secretions and atelectasis. Suctioning may be indicated,.

If the patient cannot cough effectively, chest physical therapy and assisted coughing may be indicated. Speciﬁc breathing exercises are supervised by the nurse to increase the strength and endurance of the inspiratory muscles,. Assisted coughing promotes clearing of secretions from the upper respiratory tract and is similar to using abdominal thrusts to clear an airway (see Chap. 25). It is ensure proper humidiﬁcation and hydration to prevent secretions from becoming thick and difﬁcult to remove even with coughing.

IMPROVING MOBILITY Proper body alignment is maintained at all times. The patient is repositioned frequently and is assisted out of bed as soon as the spinal column is stabilized. The feet are prone to footdrop ; therefore, various types of splints are used to prevent footdrop .. monitoring of blood pressure when positions are changed. Usually the patient is turned every 2 hours. Contractures and other complications may be prevented by range-of-motion exercises that help preserve joint motion and stimulate circulation

PROMOTING ADAPTATION TO SENSORY AND PERCEPTUAL ALTERATIONS the nurse assists the patient to compensate for sensory and perceptual alterations that occur with SCI. The intact senses above the level of the injury are stimulated through touch, aromas, flavorful food and beverages, conversation, and music. Additional strategies include the following: • Encouraging use of hearing aids, • Providing emotional support to the patient

MAINTAINING SKIN INTEGRITY . The patient’s position is changed at least every 2 hours . Careful inspection of the skin is made each time the patient is turned. The skin over the pressure points is assessed for redness or breaks . The patient’s general body align- ment and comfort are assessed.

MAINTAINING URINARY ELIMINATION . Intermittent catheterization is carried out to avoid over- distention of the bladder and UTI. If this is not feasible, an in- dwelling catheter is inserted temporarily.. The patient is taught to record ﬂuid intake, voiding pattern, amounts of residual urine after catheterization, characteristics of urine, and any unusual sensations that may occur

IMPROVING BOWEL FUNCTION a nasogastric tube is often required to relieve distention and prevent aspiration. , the patient is given a high-calorie, high-protein, high- ﬁber diet, with the amount of food gradually increased. administers prescribed stool softeners to counteract the effects of immobility and pain med-# ications .

PROVIDING COMFORT MEASURES After cervical injury, if pins, tongs, or calipers are in place, the skull is assessed for signs of infection, including drainage. The back of the head is checked periodically for signs of pressure, with care taken not to move the neck..

SURGICAL MANAGEMENT Surgery is indicated in any of the following instances: • Compression of the cord is evident. • The injury results in a fragmented or unstable vertebral body. • The injury involves a wound that penetrates the cord. • There are bony fragments in the spinal canal. • The patient’s neurologic status is deteriorating.

complications neurogenic shock Deep venous Thrombosis Respiratory failure Pneumonia Autonomic dysreflexia

NURSING DIAGNOSES Ineffective breathing patterns related to weakness or paralysis of abdominal and intercostal muscles and inability to clear secretions Ineffective airway clearance related to weakness of intercostal muscles Impaired physical mobility related to motor and sensory impairment Disturbed sensory perception related to motor and sensory impairment Risk for impaired skin integrity related to immobility and sensory loss

Assignment: Read and make notes on paraplegia, hemiplegia and quadriplegia and spinal disc problems.

CHRONIC NEUROLOGICAL CONDITIONS

SEIZURES Seizures are episodes of abnormal motor, sensory, autonomic, or psychic activity (or a combination of these) resulting from sudden excessive discharge from cerebral neurons. A part or all of the brain may be involved. The international classiﬁcation of seizures differentiates between two main types: partial seizures that begin in one part of the brain, and generalized seizures that involve electrical discharges in the whole brain (Chart 61-3). Most seizures are sudden and transient.

The underlying cause is an electrical disturbance in the nerve cells in one section of the brain, causing them to emit abnormal, recurring, uncontrolled electrical discharges. It is associated with loss of consciousness, excess movement or loss of muscle tone or movement, and disturbances of behavior, mood, sensation, and perception.

CAUSES idiopathic (genetic, developmental defects) acquired. hypoxemia of any cause, including vascular insufﬁciency , fever (childhood), head injury, hypertension, central nervous system infections, metabolic and toxic conditions ( eg , renal failure, hyponatremia , hypocal cemia , hypoglycemia, pesticides), brain tumor, drug and alcohol withdrawal, and allergies). Cerebrovascular disease is the leading cause of seizures in the elderly

Nursing Management During a Seizure A major responsibility of the nurse is to observe and record the sequence of symptoms. Before and during a seizure, the following are assessed and documented: The circumstances before the seizure (visual, auditory, or olfactory stimuli, tactile stimuli emotional or psychological disturbances, sleep, hyperventilation) • The occurrence of an aura (visual, auditory, or olfactory)

The ﬁrst thing the patient does in a seizure—where the movements or the stiffness starts, conjugate gaze position, and the position of the head at the beginning of the seizure. This information gives clues to the location of the seizure origin in the brain. (In recording, it is important to state whether the beginning of the seizure was observed

The type of movements in the part of the body involved The areas of the body involved The size of both pupils. Are the eyes open? Did the eyes or head turn to one side? The presence or absence of automatisms (involuntary motor activity, such as lip smacking or repeated swallowing) Incontinence of urine or stool

Duration of each phase of the seizure Unconsciousness, if present, and its duration Any obvious paralysis or weakness of arms or legs after the seizure Inability to speak after the seizure Movements at the end of the seizure Whether or not the patient sleeps afterward Cognitive status (confused or not confused) after the seizure In addition to providing data about the seizure, nursing care is directed at preventing injury and supporting the patient

Nursing Management After a Seizure After a patient has a seizure, the nurse’s role is to document the events leading to and occurring during the seizure and to prevent complications (e.g., aspiration, injury). To prevent complications, the patient is placed in the side-lying position to facilitate drainage of oral secretions and is suctioned,

Epilepsy

Introduction Epilepsy is defined as a chronic seizure disorder or group of disorders characterized by seizures that usually recur unpredictably in the absence of a consistent provoking factor

Etiology Unknown in 70% of cases Drug abuse; alcohol withdrawal Infections e.g. meningitis Metabolic disturbances fever Head trauma Brain tumor Stroke Near drowning or lack of oxygen from another cause Poisoning (e.g. lead) Complications of diabetes or pregnancy Genetic factors

Pathophysiology Messages from the body are carried by the neurons (nerve cells) of the brain by means of discharges of electrochemical energy that sweep along them. These impulses occur in bursts whenever a nerve cell has a task to perform. Sometimes these cells or groups of cells continue firing after a task is finished. During the period of unwanted discharges, parts of the body controlled by the errant cells may perform erratically. Resultant dysfunction ranges from mild to incapacitating and often causes unconsciousness. When these uncontrolled, abnormal discharges occur repeatedly, a person is said to have an epileptic syndrome

Precipitating factors Emotional stress Sleep deprivation Sleep itself Heat stress Alcohol Febrile illness Menstruation

International classification of seizures Partial seizures; ` I. simple- localized with symptoms generally without impairment of consciousness II.Complex partial seizures; with complex symptoms and impairment of consciousness 2.Generalized seizures Tonic clonic seizures Tonic seizures Clonic seizures Absence seizures Myoclonic seizures (bilaterally massive epileptic)

Generalized seizures Tonic: sustained muscle stiffening Clonic: sustained muscle contractions alternating with relaxations Tonic clonic seizures (grand mal seizures) Sudden loss of consciousness Tonic phase: rigid and falls to the ground, respiration are interrupted, back aches, lasts about 1min Clonic phase: rapid muscle jerking, muscle flaccidity, incontinence, tongue biting, tachycardia, heavy salivation Absence seizures (petit mal): alterations of consciousness lasting 10-30 seconds; characterized by staring (with occ. Eye blinking) and loss in postural tone Onset occurs from 3-16 years, disappear by 40 years

Postictal phase: after the seizure Patient is often confused and hard to arouse and may sleep for hours Some patients complain of headache, sore muscles, fatigue and depression

Clinical Manifestations Depending on the location of the discharging neurons, seizures may range from a simple staring episode to prolonged convulsive movements with loss of consciousness. The initial pattern of the seizures indicates the region of the brain in which the seizure originates. In simple partial seizures, only a finger or hand may shake, or the mouth may jerk uncontrollably.

In complex partial seizures, the person either remains motionless or moves automatically but inappropriately for time and place, or may experience excessive emotions of fear, anger,or irritability. There is involvement of more than one part of the brain. Generalized seizures Previously referred to as grand mal seizures, involve both hemispheres of the brain, causing both sides of the body to react.

STAGES OF GRAND MAL SEIZURE Prodrome stage: It occurs days or hours before the seizure activity. It is characterized by irritability or hyperactivity etc. Aura (warning)stage : It is characterised by certain unusual feelings such as peculiar sensation,funny smell, feeling nauseated, abdominal discomfort (gastric secretions) and flashing light. 3. Tonic stage : It usually lasts about 10 to 20 seconds. -All muscles become rigid, eyelids open, eyes look up and respiration stops temporarily resulting in cyanosis. -The tongue is bitten causing bleeding, which can be seen from the mouth.

4. Clonic stage : It usually lasts about 30 seconds. -It begins with muscle relaxation, which completely interrupts tonic muscle contraction. -There are brief violent muscle spasms of the whole body , frothing of the mouth and incontinence of urine and sometimes faeces as well. 5.Ictal phase : The patient goes into deep coma for minutes or hours 6 . Post ictal stage :(after the seizure).This is recovery stage, the patient starts regaining consciousness. - The patient is often confused and hard to arouse and may sleep for hours. -Many patients complain of headache, sore muscles, fatigue, and depression

Status epilepticus Acute prolonged seizure activity A series of generalized seizures that occur without full recovery of consciousness between attacks Can last at least 30 minutes even without loss of consciousness Considered a medical emergency Respiratory arrest occurs at the height of each seizure Precipitated by withdrawal of antiseizure medication, fever and concurrent infection

Diagnosis Diagnostic assessment is aimed at determining the type of seizures, their frequency and severity and the factors that precipitate them. Complete history and physical assessment is obtained Electroencephalogram (EEG) to diagnose and classify the seizure Other diagnostic evaluations include: Biochemical, hematologic and serologic studies Single photon emission computed tomography (SPECT) to identify epileptogenic zone in the brain MRI PET

MANAGEMENT OF EPILEPSY Seizure types and preferred drug treatment Seizure type Preferred agents Generalized tonic-clonic Carbamazepine Phenytoin Valproate Simple and complex partial Carbamazepine Phenytoin Absence Ethosuximide Valproate Myoclonic Valproate Clonazepam Status epilepticus (generalized) Diazepam/phenytoin Phenobarbital Lorazepam Neurology LA 194

Typical adult dose range Side effects Generic name Trade name (mg/day) Dose-dependent Idiosyncratic Carbamazepine Tegretol 600-1200 Ataxia, diplopia, nystagmus Hyponatremia, rash, aplastic anemia Phenytoin Dilantin 300-400 Ataxia, nystagmus, gingival hyperplasia Rash, lymphadenopathy Valproate Depakote 1000-2500 Gastric distress, alopecia, weight gain Tremor, hepatic failure, decreased platelets Phenobarbital Luminal 60-180 Sedation, ataxia, blurred vision Hyperactivity Primidone Mysoline 500-1500 Sedation, ataxia, blurred vision Ethosuximide Zarontin 750-1500 Ataxia, sedation, gastric distress, headache Rash Clonazepam Klonopin 15-20 Sedation, ataxia Neurology LA 195

SURGICAL MANAGEMENT Surgery is indicated for patients whose epilepsy results from intracranial tumors, abscess, cysts, or vascular anomalies. Some patients have intractable seizure disorders that do not respond to medication. There may be a focal atrophic process secondary to trauma, inflammation, stroke, or anoxia. If the seizures originate in a reasonably well-circumscribed area of the brain that can be excised without producing significant neurologic deficits, the removal of the area generating the seizures may produce long-term control and improvement.

Nursing management of seizures Provide privacy and protect the patient from curious on-lookers Ease the patient to the floor, if possible Protect the head with a pad to prevent injury (from striking a hard surface) Loosen constrictive clothing Push aside any furniture that may injure the patient during seizure If patient is on bed, remove pillows and raise side-rails If an aura precedes the seizure, insert an oral airway to reduce the possibility of tongue or cheek being bitten

Nursing care cont.d Do not attempt to pry open jaws that are clenched in a spasm to insert anything; might lead to broken teeth or injury to lips and tongue No attempt should be made to restrain the patient during the seizure because muscular contractions are strong and restraint can produce injury If possible, place the patient on one side with head flexed forward, which allows the tongue to fall forward and facilitates drainage of saliva and mucus. If suction is available, use it if necessary to clear secretions Status epilepticus is a medical emergency that requires adequate oxygenation with intravenous diazepam, loranzepam or fosphenytoin given slowly; with i.v normal saline

Patient education Encourage compliance to prescribed treatment Encourage patient to follow a regular and moderate routine lifestyle, diet, exercise and rest Advise the patient to avoid photic stimulation (bright fickering lights, television viewing); dark glasses or covering one eye may help Encourage patient to attend classes in stress management Instruct client to avoid over the counter medications unless approved by health care provider Instruct patient and family about medication side effects and toxicity Advise to take showers rather than tub baths to avoid drowning and to never swim alone Advised to keep a medication and seizure chart

Complications Permanent brain damage Difficulty learning Aspiration pneumonia Injury from falls, self inflicted bites, driving or operating machinery Medication side effects

Chronic degenerative disorders

Multiple sclerosis

Multiple sclerosis Introduction Multiple sclerosis (MS) is an immune-mediated progressive demyelinating disease and neurodegenerative ds of the CNS Immune system attacks cells in the protective myelin sheath that surrounds the nerve in brain and spinal cord. The damage interrupts nerve signals from brain to other parts of the body.eventualy it can cause permanent damage or deterioration of the nerves Most common age of occurrence between 20-40 Females are more affected than males

Multiple sclerosis Pathophysiology Autoimmune response results in damage and lost fibres Nerves can regain myelin, but process is not fast enough to avoid the deterioration that occurs Astrocytes form scars where myelin formerly existed Inflammation, loss of myelin and nerve fibers and scarring that follows result in reduced transmission of nerve signals within the CNS Types of symptoms and severity vary widely due to the location of the scar tissue and extent of demyelination

Multiple sclerosis Types Relapsing remitting disease: progression is characterized by relapses of active disease with incomplete recovery during periods of remission Secondary progressive disease: progression becomes more aggressive so that a consistent worsening of function occurs Primary progressive disease: symptoms are progressive from the onset of disease with early onset of disability

Etiology/ risk factors Genetic factors Gender: women are 2-3 times more at risk Race: appears more commonly in Caucasians Environmental factors: occurs commonly in northern climates(temperate climate) Socioeconomic status: least common in rural and lower class Infections; provoked by infections epstein barr virus Low levels of vit D Smoking

Clinical presentation Weakness, numbness, tingling or unsteadiness of the limbs is the most common sign Loss of balance and co-ordination Muscle weakness Spastic paralysis Urinary urgency or retention, blurry vision and double vision are common manifestations Symptoms may persist for several weeks or may resolve spontaneously over a few days

Other symptoms Speech and swallowing problems Cognitive dysfunction Difficulty in walking Bladder and bowel dysfunction Sexual dysfunction Mood swings/ depression

Multiple sclerosis.. Diagnosis Neurological examination and brain MRI scans Family history Electrophoresis of CSF identifies the presence of antibodies & immunogloulins G ( IgG )

Medical Management No cure exists for MS. An individualized, organized, and rational treatment program is indicated to relieve the patient’s symptoms and provide continuing support, particularly for individuals with cognitive changes , who may need more structure and support. The goals of treatment are to delay the progression of the disease, manage chronic symptoms, and treat acute exacerbations.

Multiple sclerosis… Treatment The interferons beta-1a and beta-1b reduce the frequency of relapse by 30% and decrease the appearance of new lesions. Pain secondary to trigeminal neuralgia can be treated with carbamazepine, gabapentin, phenytoin, pregabalin or tricyclic antidepressants The length and intensity of an acute exacerbation is shortened by the administration of glucocorticoids. An exacerbation is treated with 3 days of intense IV steroids followed by a course of oral medication tapered over 4 weeks In patients with severe disease who are unresponsive to steroid therapy, plasma exchange can be used as an alternative treatment

NURSING DIAGNOSES Impaired physical mobility related to weakness, muscle paresis, spasticity Risk for injury related to sensory and visual impairment Impaired urinary and bowel elimination (urgency, frequency, incontinence, constipation) related to nervous system dysfunction Impaired speech and swallowing related to cranial nerve involvement Disturbed thought processes (loss of memory, dementia,euphoria ) related to cerebral dysfunction Ineffective individual coping related to uncertainty of course of MS

Complications Muscle stiffness Paralysis Bladder and bowel problems Mental changes i.e. forgetfulness Depression Epilepsy

Parkinson’s disease It caused when dopamine producing neurones are in substantia nigra damaged and die overtime leading to number of motor and mental disabilities. Substantia nigra is part of basal ganglia that inhibit unwanted motor activity. When a person wants to make movement the inhibiton is removed by dopamine Low level of dopamine make it harder to initiate voluntary movement

PARKINSON’S DISEASE Parkinson’s disease is a slowly progressing neurologic movement disorder that eventually leads to disability. The degenerative or idiopathic form is the most common; There is also a secondary form with a known or suspected cause. Although the cause of most cases is unknown, research suggests several causative factors, including genetics, atherosclerosis excessive accumulation of oxygen free radicals viral infections, head trauma

chronic antipsychotic medication use, and some environmental exposure Parkinsonian symptoms usually ﬁrst appear in the ﬁfth decade of life Parkinson’s disease affects men more frequently than women and nearly 1% of the population older than 60 years o fage

There are two major neuropathologic findings in Parkinson disease 1. loss of pigmented dopaminergic neurons of substantia nigra 2. the presence of lewy bodies an ( abnormal aggregates of protein that develop inside nerve cells

Pathophysiology Parkinson’s disease is associated with decreased levels of dopamine due to destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia of the brain . The nuclei of the substantia nigra project ﬁbers or neuronal pathways to the corpus striatum, where neurotransmitters are key to control of complex body movements.

Through the neurotransmitters acetylcholine (excitatory) and dopamine (inhibitory), striatal neurons relay messages to the higher motor centers that control and reﬁne motor movements. The loss of dopamine stores in this area of the brain results in more excitatory neurotransmitters than inhibitory neurotransmitters, leading to an imbalance that affects voluntary movement

Clinical Manifestations Parkinson’s disease has a gradual onset and symptoms progress slowly over a chronic, prolonged course. The three cardinal signs are tremors- usualy begins in a limb you may rub your thumb and fore finger back and forth or hands tremble at rest , rigidity , bradykinesia (abnormally slow movements)- simple tasks difficult and time consuming.steps become shorter when walking ,dragging of feet as you walk

Other features include hypokinesia ( partial or complete loss of muscle movement due to disruption in basal ganglia, gait disturbances, and postural instability. micrographia (shrinking, slow handwriting) develops. The face becomes increasingly masklike and expressionless and the frequency of blinking decreases. Dysphonia (soft, slurred, low-pitched, and less audible speech) may occur due to weakness and incoordination of the muscles responsible for speech. In many cases, the patient develops dysphagia , begins to drool, and is at risk for choking and aspiration. .

postural and gait problems. There is a loss of postural reﬂexes , and the patient stands with the head bent forward . The patient may walk faster and faster, trying to move the feet forward under the body’s center of gravity ( shufﬂing gait). Difﬁculty in pivoting and loss of balance Psychiatric changes . -dementia (progressive mental deterioration), sleep disturbances, and hallucinations

Assessment and Diagnostic Findings patient’s history the presence of two of the three cardinal manifestations: tremor, muscle rigidity, and bradykinesia . Laboratory tests and imaging studies are not helpful in the diagnosis of Parkinson’s disease, although PET scanning has been used in evaluating levodopa (precursor of dopamine) uptake and conversion to dopamine in the corpus striatum Medical Management Treatment is directed at controlling symptoms and maintaining functional independence because there are no medical or surgical approaches that prevent disease progression.

Antiparkinsonian Medications. Levodopa ( Dopar , Larodopa ) is the most effective agent and the mainstay of treatment. Levodopa is usually given in combination with carbidopa ( Sinemet ), which prevents early conversion to dopamine and lessen side effects Anticholinergic Therapy. Anticholinergic agents ( trihexyphenidyl,cycrimine , procyclidine , biperiden , and benztropine mesylate ) are effective in controlling tremor and rigidity .

They may be used in combination with levodopa . They counteract the action of the neurotransmitter acetylcholine. Dopamine Agonists. Bromocriptine mesylate and pergolide (ergot derivatives) are dopamine receptor agonists and are useful in postponing the initiation of carbidopa or levodopa therapy. Dopamine agonists are often added to the medication regimen when carbidopa or levodopa loses effectiveness Antidepressants. Tricyclic antidepressants may be prescribed to alleviate the depression that is so common in Parkinson’s disease.

MAO inhibitors help to prevent breakdown of brain dopamine SURGICAL MANAGEMENT: Deep brain stimulation surgeons implant electrodes into a specific part of the brain and connected to a generator in the chest that send electrical impulses to the brain

NURSING PROCESS Assessment Assessment focuses on how the disease has affected the patient’s activities of daily living and functional abilities. Patients are observed for degree of disability and the functional changes that occur throughout the day, such as responses to medication. Nearly every patient with a movement disorder has some functional alteration and may have some type of behavioral dysfunction.

NURSING DIAGNOSES Impaired physical mobility related to muscle rigidity and motor weakness Self-care deficits (feeding, dressing, hygiene, and toileting) related to tremor and motor disturbance Constipation related to medication and reduced activity Imbalanced nutrition, less than body requirements, related to tremor, slowness in eating, difficulty in chewing and swallowing.

AMYOTROPHIC LATERAL SCLEROSIS Amyotrophic lateral sclerosis (ALS) is a disease of unknown cause in which there is a loss of motor neurons (nerve cells controlling muscles) As these cells die, the muscle ﬁbers that they supply undergo atrophic changes. Neuronal degeneration may occur in both the upper and lower motor neuron systems. Several theories exist regarding the cause of ALS, including autoimmune disease and free radical damage. The leading theory held by researchers is that overexcitation of nerve cells by the neurotransmitter glutamate leads to cell injury and neuronal degeneration. ALS affects more men than women, with onset occurring usually in the fifth or sixth decade.

Clinical Manifestations depend on the location of the affected motor neurons, because speciﬁc neurons activate speciﬁc muscle fibers. The chief symptoms are fatigue, progressive muscle weakness, cramps, fasciculations (twitching), and incoordination Loss of motor neurons in the anterior horns of the spinal cord results in progressive weakness and atrophy of the muscles of the arms, trunk, or legs. Spasticity usually is present, and the deep tendon stretch reﬂexes become brisk and overactive..

In about 25% of patients, weakness starts in the muscles sup-plied by the cranial nerves, and there is difﬁculty talking, swallowing, and ultimately breathing. Eventually, respiratory function is compromised. The prognosis generally is based on the area of the CNS in- volved and the speed with which the disease progresses. Death usually occurs as a result of infection, respiratory failure, or aspiration..

Management There is no speciﬁc therapy for ALS. The main focus of medical and nursing management is on interventions to maintain or improve function, well-being, and quality of life The medication riluzole ( Rilutek ), a glutamate antagonist, slows the deterioration of motor neurons.). Symptomatic treatment and rehabilitativ e measures are employed to support the patient and improve the quality of life

Most patients with ALS are managed at home and in the community, with hospitalization for acute problems. The most common reasons for hospitalization are dehydration and malnu - trition , pneumonia, and respiratory failure

Management Enteral nutrition via percutaneous endoscopic gastrostomy to stabilize body weight in patients with impaired oral intake Mechanical ventilation Mechanical insufflation.exsufflation is considered to clear secretions in patients with reduced peak cough flow Muscle relaxants to relieve spasticity Mucolytics for thickened secretions Loraxepam for anxiety Nonsteroidal anti inflammatory drugs Selective serotonin reuptake inhibitors for depression

Assignment: Read and make notes on dementia

ALZHEIMER’S DISEASE Alzheimer’s disease, or senile dementia of the Alzheimer’s type, is an acquired chronic, progressive, and degenerative brain disorder accompanied by cognitive and behavioural impairement and markedly interferes with social and occupational functioning . About 10% of the population older than age 65 are af - fected , and the prevalence reaches 47% by age 85 It is an incurable disease with a long progressive course. Research suggests that inﬂammation plays a role in the pathophysiology of the Disease

In AD plaques develops in the hippocampus a structure deep in the brain that helps encode memory & in other areas of the cerebral cortex used in thinking and making decisions

RISK FACTORS Advanced age Family history vascular factors Inflammatory markers Traumatic brain injury Signs and symptoms Memory loss Confusion about location of familiar places Taking longer to accomplish normal daily tasks They may repeat the same stories Compromised judgment Mood and personality changes increased anxiety Shortened attention span

Continuation Difficulty with language Hallucinations delusions, irritability Weight loss,seizures,lack of bladder and bowel control The patient is often unable to recognize the consequences of his or her actions and will therefore exhibit impulsive behavior.

. Personality changes are also usually evident. The patient may become depressed, suspicious, paranoid, hostile, and even combative. Progression of the disease intensifies the symptoms: speaking skills deteriorate to nonsense syllables, agitation and physical activity increase, and the patient may wander at night. Eventually, assistance is needed for most ADLs, including eating and toileting, since dysphagia occurs and incontinence develops.

Medical Management tacrine hydrochloride (Cognex). This agent enhances acetylcholine uptake in the brain, thus maintaining memory skills for a period of time. donepezil (Aricept), a second medication in this category of acetylcholinesterase inhibitors, was introduced. rivastigmine (Exelon)

Managemaent Antidepressants Anxiolytics Antiepileptic drugs Neuroleptics

Nursing Management Nursing interventions are aimed at maintaining the patient’s physical safety; reducing anxiety and agitation; improving communication; promoting independence in self-care activities; providing for the patient’s needs for socialization, self-esteem, and intimacy; maintaining adequate nutrition; managing sleep pattern disturbances; and supporting and educating family caregivers.

SUPPORTING COGNITIVE FUNCTION As the patient’s cognitive ability declines, the nurse provides a calm, predictable environment that helps the person interpret his or her surroundings and activities. Environmental stimuli are limited, and a regular routine is followed. A quiet, pleasant manner of speaking, clear and simple explanations, and use of memory aids and cues help to minimize confusion and disorientation and give the patient a sense of security. Prominently displayed clocks and calendars may enhance orientation to time.

PROMOTING PHYSICAL SAFETY A safe environment allows the patient to move about as freely as possible and relieves the family of constant worry about safety. prevent falls and other injuries, all obvious hazards are removed. REDUCING ANXIETY AND AGITATION Despite profound cognitive losses, the patient will, at times, be aware of his or her rapidly diminishing abilities. The patient will need constant emotional support that reinforces a positive selfimage .

IMPROVING COMMUNICATION To promote the patient’s interpretation of messages, the nurse remains unhurried and reduces noises and distractions. The nurse uses clear, easy-to-understand sentences to convey messages, because the patient frequently forgets the meaning of words or has difficulty organizing and expressing thoughts. PROMOTING INDEPENDENCE IN SELF-CARE ACTIVITIES. simplify daily activities by organizing them into short, achievable steps so that the patient experiences a sense of accomplishment.. Direct patient supervision is sometimes necessary, but maintaining personal dignity and autonomy is important for the person with Alzheimer’s disease.

PROVIDING FOR SOCIALIZATION AND INTIMACY NEEDS Because socialization with old friends can be comforting, visits, letters, and phone calls are encouraged. Visits should be brief and nonstressful PROMOTING ADEQUATE NUTRITION Mealtime can be a pleasant, social occasion or a time of upset and distress, so it should be kept simple and calm, without confrontation PROMOTING BALANCED ACTIVITY AND REST. It is imperative that caregivers seek to learn the needs of the patient who is exhibiting this type of behavior, because further health decline can ensue if the source of the problem is not corrected

Peripheral nerve disorders

Guillain Barre Syndrome Guillain-Barre syndrome is an autoimmune attack of the peripheral nerve myelin. The result is acute, rapid segmental demyelination of peripheral nerves and some cranial nerves, producing ascending weakness with dyskinesia (inability to execute voluntary movements), hyporeflexia, and paresthesias (numbness). In majority of the cases, there is a predisposing event, most often a respiratory or gastrointestinal infection.

The antecedent event usually occurs 2 weeks before symptoms begin. Weakness usually begins in the legs and progresses upward for about 1 month. Maximum weakness varies but usually includes neuromuscular respiratory failure and bulbar weakness. The duration of the symptoms is variable: complete functional recovery may take up to 2 years

Pathophysiology Myelin is a complex substance that covers nerves, providing insulation and speeding the conduction of impulses from the cell body to the dendrites. The cell that produces myelin in the peripheral nervous system is the Schwann cell. In Guillain-Barré the Schwann cell is spared, allowing for remyelination in the recovery phase of the disease.

Clinical Manifestations muscle weakness and diminished reflexes of the lower extremities. Hyporeflexia and weakness progress and may result in quadriplegia. Demyelination of the nerves that innervate the diaphragm and intercostal muscles results in neuromuscular respiratory failure Cranial nerve demyelination can result in a variety of clinical manifestations ( facial droop,dipolopias , dysphagia Optic nerve demyelination may result in blindness. Autonomic changes includes tachycardia, bradycardia,urinary retention Respiratory complains include dyspnea on exertion,shortness of breath, slurred speech

Bulbar muscle weakness related to demyelination of the glossopharyngeal and vagus nerves results in an inability to swallow or clear secretions Assessment and Diagnostic Findings The patient presents with symmetric weakness, diminished reflexes,and upward progression of motor weakness. A history of a viral illness in the previous few weeks suggests the diagnosis. Pulmonary function test to check for diaphragmatic strength, and respiratory muscle strength CSF studies most pts with GBS have elevated protein level with normal CSF counts

Medical Management Because of the possibility of rapid progression and neuromuscular respiratory failure, Guillain-Barré is a medical emergency, requiring intensive care unit management. Careful assessment of changes in motor weakness and respiratory function alert the clinician to the physical and respiratory needs of the patient. Respiratory therapy or mechanical ventilation may be necessary to support pulmonary function and adequate oxygenation. ( cardiac monitoring) Physical occupational and speech therapy

Other interventions are aimed at preventing the complications of immobility. These may include the use of anticoagulant agents (LMWH) and thigh-high elastic compression stockings to prevent thrombosis and pulmonary emboli. Plasmapheresis and IVIG are used to directly affect the peripheral nerve myelin antibody level . Monitoring for infectious complications e.g pneumonia, septicemia, UTIs

NURSING PROCESS ASSESSEMENT Ongoing assessment for disease progression is critical. The patient is monitored for life-threatening complications (respiratory failure, cardiac dysrhythmias , DVTs) so that appropriate interventions can be initiated. NURSING DIAGNOSES Ineffective breathing pattern and impaired gas exchange related to rapidly progressive weakness and impending respiratory failure

Impaired physical mobility related to paralysis Imbalanced nutrition, less than body requirements, related to inability to swallow Impaired verbal communication related to cranial nerve dysfunction Fear and anxiety related to loss of control and paralysis POTENTIAL COMPLICATIONS Respiratory failure Autonomic dysfunction

Disorders of neuromuscular junction

Myasthenia Gravis Myasthenia gravis, an autoimmune disorder affecting the myoneural junction, is characterized by varying degrees of weakness of the voluntary muscles. Pathophysiology Normally, a chemical impulse precipitates the release of acetylcholine from vesicles on the nerve terminal at the myoneural junction. The acetylcholine attaches to receptor sites on the motor end plate, stimulating muscle contraction.

Continuous binding of acetylcholine to the receptor site is required for muscular contraction to be sustained. In myasthenia gravis, autoantibodies directed at the acetylcholine receptor sites impair transmission of impulses across the myoneural junction Therefore, fewer receptors are available for stimulation, resulting in voluntary muscle weakness that escalates with continued activity. Eighty percent of persons with myasthenia gravis have either thymic hyperplasia or a thymic tumor , and the thymus gland is believed to be the site of antibody production.

Clinical Manifestations Diplopia (double vision) and ptosis (drooping of the eyelids) are initial symptoms. Majority of patients also experience weakness of the muscles of the face and throat (bulbar symptoms) and generalized weakness. Weakness of the facial muscles will result in a bland facial expression. Laryngeal involvement produces dysphonia (voice impairment) and increases the patient’s risk for choking and aspiration. NB: Myasthenia gravis is purely a motor disorder with no effect on sensation or coordination

Assessment and Diagnostic Findings An anticholinesterase test is used to diagnose myasthenia gravis. Anticholinesterase agents stop the breakdown of acetylcholine,thereby increasing acetylcholine availability. Edrophonium chloride ( Tensilon ) is injected intravenously, 2 mg at a time to a total of 10 mg. Thirty seconds after injection, facial muscle weakness and ptosis should resolve for about 5 minutes Atropine 0.4 mg should be available to control the side effects of edrophonium , which include bradycardia , sweating, and cramping.

Medical Management Management of myasthenia gravis is directed at improving function and reducing and removing circulating antibodies. Therapeutic modalities include administration of anticholinesterase agents and immunosuppressive therapy, plasmapheresis , and thymectomy . Pharmacologic therapy Anticholinesterase agents such as pyridostigmine bromide ( Mestinon ) and neostigmine bromide (Prostigmin) provide symptomatic relief by increasing the relative concentration of available acetylcholine at the neuromuscular junction.

Dosage is increased gradually until maximal benefits are obtained. Adverse effects of anticholinesterase therapy include abdominal pain, diarrhea, nausea, and increased oropharyngeal secretions. Cytotoxic medications have also been used, although the precise mechanism of action in myasthenia is not fully understood. Medications such as azathioprine , cyclophosphamide , and cyclosporine reduce the circulating antiacetylcholine receptor antibody titers.

PLASMAPHERESIS :Plasma exchange ( plasmapheresis ) is a technique used to treat exacerbations. IV immune globulin (IVIG) has recently been shown to be nearly as effective as plasmapheresis in controlling symptom exacerbation. SURGICAL MANAGEMENT Thymectomy (surgical removal of the thymus gland) can produce antigen-specific immunosuppression and result in clinical improvement. It can decrease or eliminate the need for medication.

Myasthenic Crisis A myasthenic crisis is an exacerbation of the disease process characterized by severe generalized muscle weakness and respiratory and bulbar weakness that may result in respiratory failure. Crisis may result from disease exacerbation or a specific precipitating event. The most common precipitator is infection; others include medication change, surgery, pregnancy, and high environmental temperature.

Neuromuscular respiratory failure is the critical complication of crisis. Respiratory muscle and bulbar weakness combine to cause respiratory compromise.

Management Neostigmine methylsulfate (PMS-Neostigmine, Prostigmin) is administered intramuscularly or intravenously until the patient is able to swallow oral anticholinesterase medications.

Plasmapheresis and IVIG, which reduce the antibody load, also may be used to treat myasthenic crisis Respiratory support and airway protection are key interventions for the nurse caring for the patient in crisis. Endotracheal intubation and mechanical ventilation may be needed . Nutritional support may be needed if the patient is intubated for a long period.

Nursing Management Because myasthenia gravis is a chronic disease and most patients are seen on an outpatient basis, much of the nursing care focuses on patient and family teaching. Educational topics for outpatient self-care include medication management, energy conservation, strategies to help with ocular manifestations, and prevention and management of complications

Bell’s Palsy Bell’s palsy (facial paralysis) is due to unilateral inflammation of the seventh cranial nerve, which results in weakness or paralysis of the facial muscles on the affected side. The cause is unknown, although possible causes may include vascular ischemia,viral disease (herpes simplex, herpes zoster), autoimmune disease ,or a combination of all of these factors.

The inflamed, edematous nerve becomes compressed to the point of damage, or its nutrient vessel is occluded, producing ischemic necrosis of the nerve. There is distortion of the face from paralysis of the facial muscles; increased lacrimation (tearing); and painful sensations in the face, behind the ear, and in the eye. The patient may experience speech difficulties and may be unable to eat on the affected side because of weakness or paralysis of the facial muscles.

Management The objectives of treatment are to maintain the muscle tone of the face and to prevent or minimize denervation. The patient should be reassured that no stroke has occurred and that spontaneous recovery occurs within 3 to 5 weeks. Corticosteroid therapy (prednisone) may be prescribed to reduce inflammation and edema; this reduces vascular compression and permits restoration of blood circulation to the nerve.

Facial pain is controlled with analgesic agents Although most patients recover with conservative treatment, surgical exploration of the facial nerve may be indicated in patients who are suspected of having a tumor or for surgical decompression of the facial nerve and for surgical treatment of a paralyzed face.

Assignment: Read and make notes on cerebral palsy, poliomyelitis and muscular dystrophy.

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