Done by: AL- Yqdhan AL- Atbi 81559 Approach to A Patient Presenting With Hemiplegia
OUTLINE Brief anatomy and physiology of brain lobes and their blood supply Different terminology Causes of hemiplegia: Stroke in details Approach to a patient presenting with hemiplegia History taking Physical examination Investigation A case: brain storming
Brain blood supply ICA Vertebral.a Hypophyseal.a Ophthalmic. a Antrerior choroidal.a Supply:optic tract, coridal plexus, internal capsule, globus pallidus ACA Supply medial aspect of frontal and parital lobe Upper lateral part of cortex of both lobes MCA Supply the whole lateral surface of parietal, temporal ,and frontal lobe Anterior and posterior spinal. a Supply spinal cord Ant & post inferior cerebellar.a Sperior cerebellar . a Supply cerebellum PCA Occipital lobe Inferomedial aspect of temporal lobe Basilar. a
BLOOD SUPPLY OF BRAIN
Anterior Limb - Frontopontine fibres , Thalamocortical fibres to frontal lobe Genu - Corticonuclear / corticobulbar fibres and Corticospinal fibres to head and neck Posterior Limb - Corticospinal fibres to trunk, upper and lower limbs, corticorubral fibres , temporopontine , parietopontine and occipitopontine fibres , thalamocortical fibres to temporal, parietal and occipital lobes Retrolentiform part -Optic radiations from lateral geniculate body (thalamus) to Visual cortex in occipital lobe Sublentiform part -Auditory radiations from Medial geniculate body (thalamus) to auditory cortex in temporal lobe
DIFFERENT TERMIMOLOGIES Paresis : partial or incomplete paralysis Plegia : complete paralysis Monoplegia is a paralysis of a single limb, usually an arm Hemiplegia : total paralysis of the arm, leg, and trunk on the same side of the body. Paraplegia : an impairment in motor or sensory function of the lower extremities. Triplegia : is paralysis of three limbs . Quadriplegia : is paralysis of all limbs, paraplegia is similar but does not affect the arms
Causes of hemiplegia
STROKE
Definitions Stroke: Clinical syndrome of rapid onset of focal deficits of brain function lasting more than 24 hours or leading to death Transient Ischemic attack (TIA): Clinical syndrome of rapid onset of focal deficits of brain function which resolves within 24 hours Amaurosis fugax
DefinitioNS Progressive Stroke: A stroke in which the focal neurological deficits worsen with time Also called stroke in evolution Completed Stroke: A stroke in which the focal neurological deficits persist and do not worsen with time
Epidemiology Third most common cause of death after cancer and ischeamic heart disease Most common cause of severe physical disability Incidence and prevalence of stroke is on the rise due to increasing adoption of unhealthy lifestyle & an increasing life expectancy
Ischemic Stroke 80% of strokes Arterial occlusion of an intracranial vessel leads to hypoperfusion of the brain region it supplies three etiological types: Thrombotic Embolic Systemic hypoperfusion
ATP depletion Hypoperfusion Failure of Na + /K + ATPase membrane ionic pump Calcium entry Glutamate release Activation of lipid peroxidases, proteases & NO synthase Destruction of intracellular organelles, cell membrane & release of free radicals Free fatty acid release Activation of pro-coagulant pathways Liquefactive necrosis Thrombus/embolus Membrane depolarization & cytotoxic cellular edema Pathophysiology of Ischemic stroke
Hemorrhagic Stroke Four types: Epidural Subdural Subarachnoid √ Intraparenchymal √ Higher mortality rates when compared to ischemic stroke
Intracerebral Hemorrhage Result of chronic hypertension Small arteries are damaged due to hypertension In advanced stages vessel wall is disrupted and leads to leakage Other causes: amyloid angiopathy , anticoagulant therapy, cavernous hemangioma , cocaine, amphetamines
Subarachnoid Hemorrhage Most common cause is rupture of saccular or Berry aneurysms Other causes include arteriovenous malformations, angiomas , mycotic aneurysmal rupture etc. Associated with extremely severe headache
Approach to A Patient Presenting With Hemiplegia
History taking The history and physical examination should be used to distinguish between other disorders in the differential diagnosis of brain ischemia . As examples, seizures, syncope, migraine, and hypoglycemia can mimic acute ischemia. It is important to ask the patient or a relative whether the patient takes insulin or oral hypoglycemic agents, has a history of a seizure disorder or drug overdose or abuse, medications on admission, recent trauma, or hysteria. The history is also important in separating ischemia from hemorrhage and distinguishing between subtypes of ischemia and hemorrhage.
History taking in hemiplegia When did the event started? What is the total duration of the illness? If multiple, ask about each episodes. What according to the patient or relatives were the initial presenting symptoms? What was the exact mode of onset: was it abrupt, sudden, sub-acute, or gradual? When was the maximum deficit noted: in the beginning or later. Time course of the initial symptoms? Static or progress Any associated symptoms: CVS,RS,or GIT?
History specific for assessing the CNS function? Was there any loss of consciousness/ in the beginning or later;did he recover from it? And for how long he stays unconsciousness? What is the emotional status of the patient; memory and intellegance ? Is speech affect and if so in what way? Motor, sensory, conductive aphasia? Which of the cranial nerve is affected and what are the symptoms related? What is the degree of motor weakness? Are you able to wear your cloths? put button of your clothes? eat? Open the door? Are you able to stand? Walk? Move your limbs? are all the modalities of sensations normally appreciated or are they abnormal?
1- Is the patient having neurological problem? Yes or no? Is it a medical condition simulating hemiplegia? Post icteal Todd’s paralysis, or episode of MS If yes, what are the neurological deficits: Hemiplegia, UMN facial weakness, hemianesthesia, homonymous hemianopia Dysphasia in right hemiplegia and dysarthria in a left hemiplegia Crossed hemiplegia Cervical cord lesion
2-Which are the CNS structures involved? Cerebral cortex Pyramidal tract Extra-pyramidal tract Cerebellum Brain stem nuclei Cranial nerve
3- Is it a UMN lesion or a LMN lesion? UMN Disease LMN Disease Suprasegmental Segmental 1. Weakness of the functional group of muscles (depending on the site of lesion). 1. Weakness in one or more muscles, depending the segmental involvement. 2. Spastic paralysis. 2. Flaccid paralysis. 3. Hypertonia. 3. Hypotonia (may be atonia if the destruction is complete). 4. Hyperreflxia (Exaggerated Deep Tendon Reflexes “DTRs”). 4. Deep Tendon Reflexes (DTRs) are lost in sever cases (decreased otherwise). 5. Positive Babinski’s sign (Extensor plantar reflex: dorsiflexion of foot). Triple Flexion: dorsiflexion of foot, leg and thigh). 5. Babinski’s sign is absent. 6. Disuse atrophy. 6. Neurogenic atrophy (denervation atrophy) about 70% - 80%. 7. Nerve conduction is normal. 7. Nerve conduction is abnormal. 8. No fibrillations or fasciculations. 8. Fibrillations and fasciculations may be present. 9. Clonus is present. 9. No clonus seen. 10. Bilateral movements such as eyes, jaws, pharynx, larynx and neck are little affected or not at all.
4- in which way the speech is effected?
5- is there a UMN or LMN facial paralysis? UMN facial paralysis: Upper half of face is spared Lower half affected no Bell’s phenomena Taste not affected LMN facial paralysis: Entire half of the face affected Bell’s phenomena present Taste affected
6- what is the site of localization of lesion?
7- is it an ischemic stroke or Hemorrhagic stroke?? Ischemic stroke Hemorrhagic stroke Start suddenly Over seconds or minutes Most cases do not progress (Complete stroke) Classically detected by patient in the morning when waking up May or may not be preceded by episodes of TIAs Mainly in HTN patients 55-75 years of age smooth onset Over minutes or hours Steady progress despite treatment Signs of increase ICT Usually associated with severe headache and vomiting
8-IF IT ISCHEMIC WHICH ARTERY INVOLVED??
9- is it internal carotid artery syndrome? Often asymptomatic Due to collaterals circulations Ext. carotid and ophthalmic anastamosis Warning symptoms: Episode of confusion Speech dysfunction Amouriosis fugax (transient mono-ocular blindness) Fleeting parasthesia Neurological deficits: Same as that of MCA territory infract Contralateral Hemiplegia Contralateral sensory symptoms Local carotid examination: Feeble carotide pulsation Feeble temporal. a pulsation Cervical bruit over carotid Carotid doppler angiography
10- which cerebral artery syndrome?
11 -
Physical Examination Level of consciousness, mental status, speech, & gait. Cranial nerves, motor function, sensory function, and superficial and deep tendon reflexes. Special reference: Optic fundus : papilledema Signs of meningeal irritation: Kernig's Signs, and Brudzinski's Sign Signs of head injury
Level f consciousness
Mental status
MOTOR FUNCTION BODY POSTURE INSPECTION- MUSCLE BULK TONE POWER REFLEXES CO-ORDINATION
SENSORY FUNCTION Pain and temperature Pressure and touch Proprioception, vibration, and fine touch
Examination of a stroke patient
Investigation All patients with suspected stroke should have the following studies immediately upon admission to the emergency department: Noncontrast brain CT or brain MRI Electrocardiogram Complete blood count including platelets Cardiac enzymes and troponin Electrolytes, urea nitrogen, creatinine Serum glucose Prothrombin time and international normalized ratio (INR) Partial thromboplastin time Oxygen saturation Lipid profile
Investigations For diagnosing ischemic stroke in the emergency setting: CT scans ( without contrast): Sensitivity : 16% Specificity : 96% MRI scan: Sensitivity : 83% specificity :98% For diagnosing hemorrhagic stroke in the emergency setting: CT scans (without contrast): Sensitivity : 89% Specificity : 100% MRI scan: Sensitivity : 81% specificity :100% For detecting chronic hemorrhages, MRI scan is more sensitive
Case1 A right handed 60 years old man was admitted with weakness involving the right side of the body. He woke up from sleep unable to move his right arm or leg. The family noted that he had right sided facial drooping. He was also noted to have difficulty speaking. No fever, headache, vomiting, seizure or loss of consciousness. He denied any chest pain or palpitation. He have an episode of weakness affecting his right arm that resolved within a few hours a few months prior to this episode. Past HX of DM and HTN for 6 years. Also diagnosed with IHD previously. On medication No history of smoking or alcohol consumption.
case1 On examination: Alert oriented and attentive Vitals: BP(180/100), RR (22), temp(36.8), O2 saturation (98%) He have: Expressive aphasia Right sided UMN seventh cranial nerve palsy Homonymous hemianopsia Dense right sided hemiplagia and hemianesthesia. Irrigulare heart sound. No murmur Destended urinary bladder
Case 1 What is the cause of his symptoms? What are the risk factors? What type of stroke he have? Which are the CNS structures involved? Which cerebral artery most likely involved? What investigation you will order?