Coma, vegetative and locked in syndrome

SandeshDahal3 713 views 34 slides Oct 11, 2020
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coma, vegetative states and locked in syndrome basic concept


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Coma, vegetative state and locked in syndrome Sandesh Dahal 2077.04.18 Introduction

Parts of consciousness Consciousness has two parts They are Wakefulness or arousal Content or Awareness to self and the environment both absent- state of coma Only wakefulness present- state of vegetative state Both present, but can’t execute motor or verbal response to them- locked in syndrome consciousness

State of consciousness after brain injury Coma Vegetative state aka unresponsive wakefulness syndrome Akinetic mutism Locked in syndrome Minimal responsive state consciousness

Coma Defects in either Thalamus bilaterally Brainstem, central upper pons or midbrain or Diffuse lesions in both cerebral hemispheres coma

State of unarousable unresponsiveness with (sedation must be excluded) Closed eyes either spontaneous or with stimuli Don’t follow commands Don’t demonstrate goal directed behavior Don’t verbalize Can’t sustain visual pursuit coma

Coma No single score defines coma. 90% of people with GCS < 8 fits into the definition. And mostly none with GCS >9 fits to this definition. So, GCS <8 is almost like operational definition of coma for practical purposes. coma

Glasgow coma scale coma

coma

E tiology Broadly can be divided into with localizing features Without localizing features Without localizing features With meningism Without meningism coma

Etiology Toxic or metabolic Electrolyte imbalance- Na, Ca, BUN, HE Endocrine- glucose, DKA, HHS, myxedema, addisonian crises Vascular- vasculitis, DIC, hypertensive encephalopathy Toxic- alcohol, drugs like narcotic overdose Infectious and inflammatory- meningitis, encephalitis, sepsis, lupus cerebritis etc coma

Neoplastic- leptomeningeal carcinomatosis Nutritional- Wernicke’s encephalopathy Metabolic diseases- porphyria, lactic acidosis Epileptic- status and post ictal state coma

causes….. Structural Vascular- Bilateral cortical or subcortical infarcts Occlusion of bilateral hemispheres eg bilateral carotid stenosis Bilateral diencephalic infarcts Infectious- abscess with mass effect, HSV encephalitis coma

Structural… Trauma- contusion, edema Neoplastic Herniations causing compression of RAS Raised ICP Acute midline shift due to hematomas coma

Vegetative state show the behaviors of arousal, but No ability to interact with the environment They may have Periods of eye opening either to stimuli or spontaneous Subcortical response to pain like posturing, tachycardia or diaphoresis Subcortical motor response like grasp reflex Brainstem functions like sleep wake or normal respiratory function, swallowing and temperature regulation is present Eye movements without visual tracking Vegetative state

Diagnosis of vegetative state Three prime features Sleep wake cycle present All the responses are identified as reflex activities No awareness and no meaningful response to stimuli ANDREWS  K, The vegetative state − clinical diagnosis, Postgraduate Medical Journal  1999; 75: 321-324. Vegetative state

The vegetative and minimally conscious states: Consensus-based criteria for establishing diagnosis and prognosis, NeuroRehabilitation 19 (2004) 293–298 293 IOS Press Giacino , Joseph T . Vegetative state

If vegetative state > 1 month- persistent vegetative state If >3 months in non traumatic injury- chronic vegetative state If >12 months in traumatic injury- chronic vegetative state Vegetative state

Locked in syndrome Its not a vegetative or coma state But it is an important differential Many cases are mistaken for diagnosis Lesion Ventral pons Results in normal dorsal midbrain and pons function Locked in syndrome

The dorsal midbrain and pons including reticular center is intact The person can feel self and environment The person is alert and aware of self and environment, but Can’t respond, because there is damage to bilateral cortiospinal and corticobulbar tracts Locked in syndrome

The only possible response is Blinking of eye- variable Up and downgaze of eye Otherwise, there is quadriparesis and inability to use the muscles of facial expression Horizontal eye gaze is not possible ‘Alphabet in the air’- communication technique Locked in syndrome

Coma- core examination Meningism Respiration Examination in coma

Cheyne -stokes- crescendo-trail off- pause Occurs in diencephalic lesions and bilateral cerebral hemispheric dysfunction Cluster breathing- rapid irregular-apneic spells Lesion in high medulla or lower pons Apneustic - pause at full inspiration Pontine lesions Ataxic/ biots breathing- no pattern in rate and depth In medullary lesion Examination in coma

Pupil Record direct and consensual light Examination in coma

Bilateral pinpoint pupil- medullary lesion Bilateral fixed and dilated- subtotal medulla damage, hypoxia and hypothermia Midposition fixed- extensive medulla damage Examination in coma

Ocular deviation Bilateral conjugate deviation- frontal lobe, looks away from destructive lesion and looks towards irritative lesion Pontine lesion- looks away from the lesion Downward deviation- perinaud syndrome Unilateral down and out- IIIrd nerve palsy, uncal herniation Unilateral inward deviation- Vith nerve palsy Examination in coma

Spontaneous eye movements Windshield wiper eyes- non localizing, but indicates IIIrd and MLF are intact Pingpong gaze- deviation to left right at 3-5/sec, and pause for 2-3 sec, indicates bilateral cerebral dysfunction. INO- ipsilateral eye cant adduct. Lesion in MLF Examination in coma

Ocular bobbing- repetitive rapid vertical down movement Occurs in brainstem lesion Oculovestibular reflex- head 30 deg , intact TM, 60-100 ml of ice water Intact brainstem- tpnic conjugate eye deviation to side of cold stimulus No response- toxic or metabolic eg barbiturates and muscle relaxants Assymmetric - infratentorial lesion Nystagmus without clonic deviation- psychogenic coma Examination in coma

Dolls eye response- don’t do if cervical spine is not ruled out Normal is contraversive eye movement Caloric absent and dolls eye present in cases of streptomycin toxicity and bilateral vestibular schwannoma Examination in coma

Motor response Asses corticospinal tract Symmetric- in metabolic causes Asymmetric – supratentorial lesions Inconsistent- seizure or psychiatric Hyporeflexia- myxedema coma Examination in coma

Posturing Decorticate- cortical or subcortical lesions Decerebrate - brainstem or below lower midbrain Arms flexed and legs flaccid- pontine tegmentum Arms flaccid legs appropriate- anoxic injury Examination in coma

Examination in coma

Ciliospinal reflex- Noxious stimuli cause pupil to dilate Bilateral- metabolic Unilateral- 3 rd nerve palsy Bilateral absent- non localizing Examination in coma

Examination in coma

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