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LOCALISATION OF LESION CAUSING COMA.pptx
- 1. LOCALISATION OF LESION CAUSINGCOMA DR VIJAY PRAKASH HAWA SR NEUROLOGY GMC KOTA
- 2. OUTLINE • COMA, AKINETICMUTISM, LOCKED IN SYNDROMES • ANATOMICAL SUBSTRATE OF ALERTNESS • SIGNS WITH LOCALIZING VALUE IN COMA • CLINICAL PRESENTATION OF COMA INDUCING LESIONS DEPENDING ON THEIR LOCATION
- 3. Consciousness defined asa state of awareness of self and surroundings. Alterations in consciousness are conceptualized into two types. The first type affects arousal The second type involves cognitive and affective mental function, sometimes referred to as the “content” of mental function.
- 5. Alterations in arousal,although often referred to as altered levels of consciousness Four points on the continuum of arousal are often used in describing the clinical state of a patient: Alert refers to a perfectly normal state of arousal. Lethargy lies between alertness and stupor. Patient Often Aroused By Verbal Stimuli Stupor is a state of baseline unresponsiveness that requires repeated application of vigorous stimuli to achieve arousal. Coma is a state of complete unresponsiveness to arousal.
- 7. Criteria for theDiagnosis of a Persistent Vegetative State 1.No evidence of awareness of themselves or their environment; they are incapable of interacting with others 2. No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, auditory, tactile, or noxious stimuli 3. No evidence of language comprehension or expression 4. Intermittent wakefulness manifested by the presence of sleep/wake cycles 5. Sufficiently preserved hypothalamic and brainstem autonomic functions to survive if given medical and nursing care 6. Bowel and bladder incontinence 7. Variably preserved cranial nerve (pupillary, oculocephalic, corneal, vestibuloocular, and gag) and spinal reflex Data from The Multi-Society Task Force on PVS. Medical aspects of the persistent vegetative state. N Engl J Med 1994;3330, 1499–1508, 1572–1579
- 8. Causes of Coma I.Symmetrical—Nonstructural Toxins Lead, Thallium, Mushrooms, Cyanide, Methanol, Ethylene glycol ,,Carbon monoxide Drugs Sedatives ,Barbiturates ,Other hypnotics Tranquilizers ,Bromides, Alcohol ,Opiates, Paraldehyde ,Salicylate Psychotropics ,Anticholinergics ,Amphetamines, Lithium, Phencyclidine, Monoamine oxidase inhibitor Metabolic Hypoxia, Hypercapnia, Hypernatremia, Hyponatremia,Hypoglycemia, Hyperglycemic nonketotic coma ,Diabetic ketoacidosis ,Lactic acidosis, Hypercalcemia, Hypocalcemia, Hypermagnesemia ,Hyperthermia ,Hypothermia ,Reye encephalopathy Aminoacidemia, Wernicke encephalopathy ,Porphyria ,Hepatic encephalopathy, Uremia ,Dialysis encephalopathy Addisonian crisis II. Symmetrical—Structural Supratentorial Bilateral internal carotid occlusion, Bilateral anterior cerebral artery occlusion III. Asymmetrical—Structural Supratentorial -Thrombotic thrombocytopenic purpura, Disseminated intravascular coagulation, Nonbacterial thrombotic endocarditis (marantic endocarditis), Subacute bacterial endocarditis, Fat emboli, Unilateral hemispheric mass (tumor, bleed) with herniation
- 9. Subarachnoid Hemorrhage Thalamic hemorrhage*Trauma—contusion, concussion* ,Hydrocephalus Subdural Hemorrhage, Bilateral Intracerebral bleed Pituitary apoplexy† Massive or bilateral supratentorial infarction Multifocal leukoencephalopathy Creutzfeldt-Jakob disease Adrenal leukodystrophy Cerebral vasculitis Cerebral abscess Infections Bacterial meningitis Viral encephalitis Postinfectious encephalomyelitis Syphilis Sepsis Typhoid fever Malaria Waterhouse-Friderichsen syndrome Psychiatric Catatonia Other Postictal Diffuse ischemia (myocardial infarction, congestive heart failure, arrhythmia) ,Hypotension, Fat embolism Hypertensive encephalopathy, Hypothyroidism, Infratentorial Basilar occlusion, Midline brainstem tumor, Pontine haemorrhage, Subdural Empyema Thrombophlebitis, Multiple sclerosis Leukoencephalopathy associated with hemotherapy, Acute disseminated encephalomyelitis ,Infratentorial Brainstem infarction, Brainstem hemorrhage.
- 10. ANATOMICAL SUBSTRATE OFALERTNESS • The maintenance of consciousness depends on interaction between the ascending reticular activating system (ARAS) and the cerebral hemispheres. • ARAS lies in the paramedian tegmental region of the posterior portion of the pons and midbrain
- 11. • complex polysynapticfiber system -extends from the superior half of the pons through the midbrain to the posterior portion of the hypothalamus and to the thalamic reticular formation. • The thalamus • -source of diffuse thalamocortical projections -regulate and coordinate cortical activity. • Sedative drugs act, at least in part, by interfering with the synaptic network of the ARAS
- 12. • Bilateral cerebralhemispheric lesions may cause transient coma, particularly when they involve the mesial frontal region. • Large unilateral lesions of the dominant hemisphere may occasionally cause transient unresponsiveness, even in the absence of a mass effect. • posterior hypothalamic lesions induce prolonged hypersomnia. • Acute bilateral damage of the paraventricular thalamic nuclei is attended by transient unresponsiveness, followed, when the lesions are large, by severe amnestic dementia
- 13. HISTORY • briefly interviewingrelatives, friends, bystanders • The patient’s wallet or purse should be examined for lists of medications, a physician’s card, or other information • patient’s social background and prior medical history and the circumstances in which the patient was found.
- 14. Signs with LocalizingValue in Coma • Respiratory pattern, • Pupillary response, • Eye movements, and • Position or movements of the limbs
- 15. Respiratory Patterns A.Cheyne-Stokes respiration-denotes a cyclic pattern of alternating hyperpnea and apnea. -bilateral hemispheric or diencephalic insult may indicate incipient transtentorial herniation - CHF,COPD,OSA, Uremia. B. Hyperventilation -injury in the pontine or midbrain tegmentum; -respiratory failure, hemodynamic shock, fever, sepsis, metabolic disarray, and psychiatric disease. C.Apneustic breathing -prolonged pause at the end of inspiration -lateral tegmentum of the lower half of the pons. D.Cluster breathing -Periodic respirations that are irregular in frequency and amplitude with variable pauses between clusters of breath -lower pontine tegmental lesion E.Ataxic breathing is irregular in both rate and tidal volume - suggests damage to the medulla.
- 16. • Temperature Changes •Pure neurogenic hyperthermia -rare -usually is due to a. subarachnoid hemorrhage b. diencephalic (hypothalamus) lesions. c. pontine tegmental lesions • Other causes of increased temperature associated with coma are heatstroke, thyrotoxic crisis, and drug toxicity. (Atropine and other anticholinergics) • hypothermia associated with coma are hypothyroid coma, hypopituitarism, Wernicke encephalopathy, cold exposure, drugs (barbiturates), and other poisonings. • Central lesions causing hypothermia are found in the posterior hypothalamus
- 17. THE PUPILS Pupillary shape,size, symmetry, and response to light provide valuable clues to brainstem and third cranial nerve function. 1.Sleep or bilateral diencephalic dysfunction (metabolic coma) -small pupils that react well to light (diencephalic pupils). 2.Unilateral hypothalamic damage - miosis and anhidrosis on the side of the body ipsilateral to the lesion.
- 18. 1. Midbrain lesions 1.Tectalor pretectal lesions affecting the posterior commissure 1. abolish the light reflex, 2.the pupils are midsized or slightly large, 3.spontaneous oscillations in size (hippus) 4. Positive ciliospinal reflex. 2. Tegmental lesions-involve the third nerve nucleus, -nonuniform paresis or paralysis of the pupil sphincter irregular constriction of the sphincter of the iris pear-shaped pupil or displacement of the pupil to one side (midbrain corectopia). The pupils, often unequal, tend to be midsized and lack light or ciliospinal responses.
- 19. 4.Pontine tegmental lesions -smallpupils due to interruption of descending sympathetic pathways. Pinpoint pupils, when observed with a magnifying glass, may be seen to constrict to light 5. Lateral pontine, lateral medullary, and ventrolateral cervical cord lesions produce an ipsilateral Horner syndrome. 6. Oculomotor nerve compression and elongation by herniation of the uncus of the temporal lobe (through the tentorial incisura) affect pupillary function earlier and more noticeably than the extrinsic eye movement
- 20.
- 21. Eye Movements • Inthe comatose patient the assessment of eye movements helps to determine the level of structural brainstem damage or the depth of coma induced by metabolic agents. • the assessment of ocular motility in comatose patients relies heavily on reflex eye movements, including • the oculocephalic reflex, elicited by the doll’s eye maneuver, • the oculovestibular reflex, elicited by instillation of cold or warm water into the external auditory canal.
- 22. Eye Movements ROVING EYEMOVEMENTS- -the eyelids are closed -the eyes slightly divergent, -drift slowly from side to side -brainstem is intact , cortical dysfunction -cannot be voluntarily executed and are therefore incompatible with the diagnosis of pseudocoma . EYES-OPEN COMA – -Spontaneous blinking requires an intact pontine reticular formation. -Absence of blinking only on one side indicates unilateral nuclear, fascicular, or peripheral facial nerve dysfunction. -The eyelids may remain tonically retracted due to failure of levator inhibition in some cases of pontine infarction.
- 24. • Short-cycle PeriodicAlternating Gaze (Ping-pong Gaze) -Roving of the eyes from one extreme of horizontal gaze to the other and back -each oscillating cycle taking 2.5 to 8 seconds. -indicates bilateral cerebral damage (e.g., bilateral cerebral infarcts) with an intact brainstem - Posterior Fossa Hemorrhage, Basal Ganglia Infarcts, Hydrocephalus -This disorder of ocular motility had no prognostic value . • Repetitive divergence -the eyes are in midposition or slightly divergent at rest. -They then slowly deviate out, become fully deviated for a brief period, and then rapidly return to the primary position before repeating the cycle. -synchronous in both eyes. -rarely seen in patients with coma from metabolic encephalopathy (e.g., hepatic encephalopathy)
- 25. • • Nystagmoid jerking ofa single eye, in a vertical, horizontal, or rotatory fashion, may occur with mid- to lower pontine damage • Electrographic status epilepticus without appendicular motor manifestations, due to anoxia, may result in brisk, small-amplitude, mainly vertical (occasionally horizontal) eye movements detectable by passive lid elevation
- 26. OCULAR BOBBING intermittent, often conjugate, brisk, bilateraldownward movement of the eyes with slow return to midposition. -Typical ocular bobbing- with preserved horizontal eye movements, specific but not pathognomonic of acute pontine injury -Atypical ocular bobbing, associated with absent horizontal eye movements, -non-localizing, can be seen in pontine lesions, extra-axial posterior fossa masses ,diffuse encephalitis ,Creutzfeldt-Jakob disease ,toxic-metabolic encephalopathies (e.g., acute organophosphate poisoning) -Monocular bobbing (paretic bobbing), may occur if there is a coexistent unilateral fascicular oculomotor nerve palsy
- 27. Inverse ocular bobbing(ocular dipping) - Slow-downward Eye Movement With Fast Return To Midposition - Occur In Anoxic Coma Or After Prolonged Status Epilepticus. - Probably Reflects Diffuse Brain Dysfunction Rather Than A Single Structural Lesion Brainstem - Horizontal Gaze Reflexes Are Usually Intact Reverse ocular bobbing -fast-upward eye movement with a slow return to midposition, -occur in patients with metabolic encephalopathy, viral encephalitis, or pontine haemorrhage
- 28. Reverse ocular dipping -slow-upwardeye movements followed by fast return to midposition -metabolic or viral encephalopathy (i.e., diffuse cerebral dysfunction). -Can be present in pontine infarction (the patient had a one-and-a-half syndrome ) Pretectal pseudobobbing in acute hydrocephalus arrhythmic, repetitive downward and inward (“V-pattern”) eye movements at a rate ranging from 1 per 3 seconds to 2 per second and an amplitude of 1/5 to 1/2 of the full voluntary range -may be mistaken for ocular bobbing - its presence usually indicates the need for prompt surgical attention (e.g., hydrocephalus decompression)
- 31. Abnormalities of LateralGaze 1.Conjugate Gaze When both eyes remain deviated toward the same side in a comatose patient, Hemispheric lesion, the eyes look toward the lesion (away from the hemiparetic side) A seizure originating in the frontal or occipital lobes may cause deviation of the eyes and head away from the lesion
- 32. WRONG-WAY EYES • forceddeviation of the eyes to the side contralateral to the lesion • Thalamic and, rarely, basal ganglionic lesions, almost always hemorrhagic, • Very rarely, frontal-perisylvian lesions Unilateral lesions affecting the tegmentum of the lower pons cause a horizontal gaze palsy toward the side of the lesion so that the eyes look toward the hemiparetic side. Coma due to toxic substances is often accompanied by impaired conjugate eye movements, horizontal as well as vertical ( Wernicke's encephalopathy)
- 33. 2. DISCONJUGATE GAZE •Isolated failure of ocular adduction, in the absence of pupillary changes and with normal vertical eye movements (elicited by oculocephalic or oculovestibular reflexes), • a lesion of the MLF in the upper pons ipsilateral to the eye that fails to adduct. • MLF involvement is commonly bilateral in comatose patients. • Latent strabismus may become apparent when the level of alertness is mildly impaired but disappears in deep coma
- 35. . Abnormalities of VerticalGaze in light coma, upward gaze can be tested by holding the eyelids open and gently touching the cornea with a wisp of cotton or a similar object. With this stimulus the eyeballs tend to roll upward (Bell phenomenon). Disconjugate vertical gaze in the resting position (skew deviation) • lesions at different areas of the brainstem, • with increased intracranial pressure, or • with hepatic coma Persistent deviation of the eyes below the horizontal meridian signifies brainstem dysfunction, • structural lesion that affects the tectum of the midbrain • occasionally by metabolic encephalopathy (e.g., hepatic coma ). • after anoxic brain damage
- 36. Thalamic Hemorrhage -Tonicdownward deviation of the eyes, often accompanied by convergence - due to pressure on the dorsal mesencephalon. Feigning Coma Forced downward deviation of the eyes has also been reported in patients Tonic up-gaze has been reported shortly after severe anoxic encephalopathy and with phenothiazine intoxication. Downward gaze is preferentially affected by bilateral lesions of the superomedial perirubral regionLarge midbrain tegmental lesions abolish vertical gaze
- 39. Corneal Reflex • Thecorneal reflex has a higher threshold in comatose patients. • Decreased corneal sensitivity cranial nerve V lesions, ipsilateral lateral pontomedullary lesions, or contralateral parietal lesions • Impaired eye closure (as with cranial nerve VII lesions and low pontine lesions). the stimulus may induce deviation of the jaw to the opposite side (corneopterygoid reflex), given an intact upper pons and midbrain, the eyes may roll upward (Bell's phenomenon
- 40. Motor Activity ofthe Body and Limbs • Less clear-cut localizing value than similar findings in alert patients. • Motor patterns, widely known as decorticate (flexor posturing) and decerebrate (extensor posturing) rigidity, are often produced by metabolic disorders • Structural damage to the origin or course of the motor pathways may give rise to such patterns, which, in these cases, are often asymmetric. • Anoxic lesions of the cerebral border zones may result in predominant damage to the cortex in the area of representation of the arms. Such patients may have bilateral arm weakness with relatively spared lower extremity function (man-in- the-barrel syndrome)
- 43. Clinical Presentations ofComa-Inducing Lesions Depending on Their Location
- 44. • The phylogeneticallynewer brain structures tend to be more sensitive to metabolic injury. • Functions subserved by complex polysynaptic pathways are affected earlier by metabolic disturbances than those mediated by a few neurons. • higher cortical functions and attention succumb early to metabolic insults, whereas the pupillary light reflex remains to the brink of brainstem death. • Asymmetric motor findings speak against the diagnosis of metabolic encephalopathy but ethylene glycol, produce focal brain injuries. Metabolic Encephalopathy (Diffuse Brain Dysfunction)
- 45. • Focal seizuresare common in metabolic encephalopathies, particularly those coursing with breakdown of the blood-brain barrier, such as eclampsia, malignant hypertension, and acute intermittent porphyria. • Toxic-metabolic disorders often induce abnormal movements (tremor, asterixis, myoclonus, and seizures) • The tremor of metabolic encephalopathy is coarse and irregular and ranges from 8 to 10 cycles per second.
- 46. • Asterixis isa sudden, brief loss of postural tone that is translated into a flapping movement when the hand is held in dorsiflexion at the wrist and the fingers are extended and abducted. Unilateral asterixis may be seen contralateral to lesions of the mesencephalon, ventrolateral thalamus, primary motor cortex, or parietal lobe or ipsilateral to lesions of the pons or medulla. bilateral asterixis may occur with bilateral lesions of the midpons or with bilateral mesencephalic lesions
- 47. Multifocal myoclonus • sudden,nonrhythmic twitching • affects first one muscle, then another, without any specific pattern except a tendency to involve the facial and proximal limb musculature. • uremic and hyperosmolar-hyperglycemic encephalopathy, carbon dioxide narcosis, and a large dose of intravenous penicillin Generalized myoclonus • usually postanoxic, • involves mainly the axial musculature, which contracts suddenly, • making the patient jump with a certain periodicity
- 48. • Autoimmune disorders 1.Antibodies against the N-methyl-D-aspartate (NMDA) receptors- Before becoming comatose, these patients typically transition to a state with psychiatric manifestations and choreic or other movement disorders 2. Antibodies against the GABA A receptor- can also cause coma and refractory status epilepticus
- 49. SUPRATENTORIAL STRUCTURAL LESIONS •To cause coma, supratentorial lesions must affect both cerebral hemispheres (e.g., massive bihemispheric or bilateral thalamic infarction) • appear more abruptly than metabolic encephalopathies, and cause asymmetric motor signs, at least early in their course. • Sudden onset of severe headache (“thunderclap headache”) and signs of meningeal irritation separate subarachnoid hemorrhage from metabolic encephalopathies
- 50. • supratentorial lesionsthat cause mass effect and secondarily impair consciousness by compressing the diencephalic and upper brainstem structures. • hemispheric tumors, subdural or intracerebral hemorrhage, and massive infarcts. • Depending on the supratentorial location of the mass and the size of the tentorial opening, either of two clinically relevant syndromes may result: A. lateral (uncal) herniation B. central (transtentorial) herniation.
- 51. A. LATERAL (UNCAL)HERNIATION
- 52. lateral extracerebral ortemporal lobe masses ↓ push the mesial temporal lobe (uncus anteriorly, parahippocampal gyrus posteriorly) between the ipsilateral aspect of the midbrain and the free edge of the tentorium ↓ compresses the third cranial nerve and posterior cerebral artery the ipsilateral pupil becomes progressively dilated and responds sluggishly to light a hemorrhagic mesial occipital infarct ↓ pushes the midbrain against the rigid edge of the dura on the opposite side of the tentorial opening ↓ carves out a notch (Kernohan's notch) in the lateral aspect of the midbrain, interrupting the cerebral peduncle (particularly the fibers that project to the leg) on the side opposite the original temporal lobe lesion ↓ hemiparesis ipsilateral to the original lesion (Kernohan's notch phenomenon)a false localizing sign ↓ tearing of the paramedian midbrain perforating vessels infarction and hemorrhages (Duret's hemorrhages) the sympathetic pathway is damaged in the midbrain pupil becomes midsize and unresponsive. ↓ Oculomotorparesis appears first in the eye originally involved and shortly afterward in the other eye
- 54.
- 55. frontal, parietal, oroccipital masses ↓ the supratentorial pressure increases ↓ first compress the diencephalon ↓ shifts downward and buckles over the midbrain ↓ Subsequent flattening of the midbrain and pons in the rostrocaudal direction ↓ causes elongation and rupture of the paramedian perforating arteries ↓ infarction and hemorrhages (Duret's) in the tegmentum of the midbrain (first) and pons(afterward) ↓ Paralleling the pathologic changes of central herniation, the clinical picture reflects an orderly rostrocaudal progression of brainstem damage
- 56. EARLY DIENCEPHALIC STAGE •Impaired attention and somnolence. • The respiratory pattern is normal but is punctuated by deep sighs and yawns. • the pupils become tiny but react to light, • the eyes become slightly divergent, moving slowly from side to side (roving eye movements). • Attempts to perform the doll’s eye maneuver may provide enough of a stimulus to awaken the patient, and quick eye movements (saccades) are then elicited rather than the slow adversive movements of the oculocephalic reflex. • The patient resists passive motion of the limbs (paratonia), may have grasp reflexes. • Plantar responses are usually bilaterally extensor.
- 58. Late Diencephalic Stage •At this stage the patient cannot be aroused. • Roving eye movements have disappeared , tectal dysfunction may result in restriction of upward gaze. • Light painful stimuli fail to elicit any response • Proper diagnosis and treatment at this stage of the syndrome of central herniation may still result in recovery of neurologic function.
- 60. Midbrain- Upper PonsStage • Temperature oscillations are common, and an occasional patient may develop diabetes insipidus because of stretching of the median eminence of the hypothalamus. • The pupils become midsized, unequal, and irregular, often pear-shaped and eccentric. • The doll's eye maneuver and caloric testing elicit restricted or no vertical eye movements. • The eyes often move disconjugately in both the horizontal and the vertical planes. • Bilateral impairment of adduction may reflect dysfunction of both third nerve nuclei, of the medial longitudinal fasciculi, or both
- 62. LOWER PONTINE STAGE •Respiration becomes quicker and shallower. • Apneustic breathing, common with primary ischemic lesions of this area, is infrequent in patients with transtentorial herniation, perhaps because more medially located structures are preferentially damaged. • The pupils remain unchanged from the previous stage, but eye movements are now unobtainable. • Decerebrate rigidity decreases. • Plantar stimulation may elicit not only bilateral Babinski signs but also withdrawal of the legs, with flexion at the knee and hip.
- 64. MEDULLARY STAGE • AtaxicBreathing Soon Gives Way To Apnea. • The Blood Pressure Drops, And • The Pulse Becomes Irregular
- 65. Lateral displacement ofthe brain and level of consciousness in patients with an acute hemispheral mass. N Engl J Med. 1986;314:953– 958.Ropper AH. • Early depression of the level of alertness in patients with an acute hemispheric mass may be more related to distortion of the brain by horizontal rather than vertical displacement of brain tissue . • Horizontal pineal body shift from the midline was associated with, 0 to 3 mm with alertness 3 to 4 mm with drowsiness, 6 to 8.5 mm with stupor, 8 to 13 mm with coma
- 66. Prognosis of lobarhemorrhages • Glasgow coma score less than 14 • Hemorrhage volume 60 ml, • Shift of the septum pellucidum, • Effacement of the contralateral ambient cistern, and • Widening of the contralateral temporal horn. Deeper putaminal hemorrhages fare worse when accompanied by hydrocephalus and the patient has a GCS score less than 8. Flemming KD, Wijdicks EF, St Louis EK, et al. Predicting deterioration in patients with lobar haemorrhages. J Neurol Neurosurg Psychiatry. 1999;66:600–605.
- 67. FALSE LOCALIZING SIGNSWITH SUPRATENTORIAL MASSES • hemiparesis ipsilateral to the lesion due to Kernohan notch • falsely localize the primary process to the posterior fossa --mainly with lesions located in the midline (e.g., hydrocephalus) or -- in areas of the frontal and temporal lobes that are clinically “silent.” Extracerebral lesions (e.g., subdural hematoma) in the elderly. • fail to cause focal deficits but raise the pressure of the intracranial contents and produce cranial nerve dysfunction that may be mistaken for evidence of a posterior fossa lesion.
- 68. • Sixth nervepalsy and papilledema are the commonest false localizing signs, • Other ophthalmoplegias, trigeminal neuralgia or numbness, unilateral or bilateral deafness, facial palsy, and even weakness in the distribution of the ninth to twelfth cranial nerves may appear as a consequence of raised intracranial pressure with a supratentorial lesion.
- 69. SUBTENTORIAL STRUCTURAL LESIONS •Early in the clinical course-occipital headache, vomiting, and ataxia are usually prominent. • Lesions that compress the upper brainstem may cause upward transtentorial herniation of the tectum of the midbrain and of the anterior cerebellar lobule giving rise to signs of midbrain dysfunction with coma hyperventilation, fixed pupils, and vertical ophthalmoplegia.
- 70. • Lower lesionsimpinge on the pontine tegmentum - somnolence, - pinpoint pupils that react briskly to light, - oculoparetic nystagmus on lateral gaze, - truncal ataxia. - Appendicular ataxia may be so mild as to pass unnoticed. • As pontine function becomes worse horizontal gaze disappears and cannot be elicited with the doll's eye maneuver or caloric testing, whereas impairment of vertical eye movements clearly lags behind.
- 71. • Anatomic findingsthat predict deterioration with cerebellar hemorrhage include • displacement of the fourth ventricle, • brainstem deformity, • hydrocephalus, and • compression of the basal cisterns. • In some series, a hematoma size of more than 3 cm also worsens prognosis. St Louis EK, Wijdicks EF, Li H, et al. Predictors of poor outcome in patients with a spontaneous cerebellar hematoma. Can J Neurol Sci. 2000;27:32–36
- 72. LESIONS THAT IMPINGEON THE MEDULLA - respiratory ataxia evolving to apnea - circulatory abnormalities precede changes in the level of alertness. • The medulla is particularly resistant to infarction, spontaneous hemorrhages, and even traumatic lesions. • However, it is preferentially affected in Listeria monocytogenes rhombencephalitis and in Leigh's disease
- 73. PSYCHOGENIC UNRESPONSIVENESS • Thepatient may hold the eyes forcibly closed and resist eyelid opening with a tendency for abrupt closure of eyelids • or may keep the eyes open in a fixed stare, interrupted by quick blinks. • The pupils, which are of normal size and position, react to light unless a cycloplegic drug has been instilled into them. • The doll's eye maneuver elicits random or no eye movements. • Caloric testing is more helpful because it gives rise to classic vestibular nystagmus with a quick component that requires activity of the frontal eye fields. This quick component is, conversely, absent in comatose patients.
- 74. • Muscle toneand reflexes are normal. • The patient may hyperventilate or breathe normally. • Eye gaze sign, in which patients tend to look to the ground when turned on to one side • Hand drop test of attentiveness • Harvey's sign- application of high-frequency vibrating tuning fork to the nasal mucosa • Yasser’s Maneuver • Psychogenic unresponsiveness often recurs and as such is frequently misdiagnosed as an epileptic or migranous disorder.
- 75. TAKE HOME MESSAGE •Rapid and proper history and examination is must in emergency room for localization of lesion causing coma. • Proper focusing on signs during examination we able to reach about temporal course, severity and nature and site of disease in most of cases . • and also able to differentiate most of times in true and pseudocoma. • we able to do appropriate and precise investigations which saves time and money both. • Proper localization help in fast and right management of patient and saving the life.
- 76. REFERENCES: 1. Bradley andDaroff’s Neurology in clinical practice,8th edition,2021 2. Brazis Localization in Clinical Neurology, 2017 3. St Louis EK, Wijdicks EF, Li H, et al. Predictors of poor outcome in patients with a spontaneous cerebellar hematoma. Can J Neurol Sci. 2000;27:32–36 4. Flemming KD, Wijdicks EF, St Louis EK, et al. Predicting deterioration in patients with lobar haemorrhages. J Neurol Neurosurg Psychiatry. 1999;66:600–605. 5. Ropper AH. Lateral displacement of the brain and level of consciousness in patients with an acute hemispheral mass. N Engl J Med. 1986;314:953– 958. 6. Data from The Multi-Society Task Force on PVS. Medical aspects of the persistent vegetative state. N Engl J Med 1994;3330, 1499–1508, 1572–1579 7. Y M H Elsayed. (2021). Yasser’s Maneuver for Regaining the Consciousness in the Psychogenic Coma; A Novel Maneuver in Emergency Medicine and Psychiatry. Journal of Clinical and Laboratory Research.
- 77.
Editor's Notes
- #4 Sleep, the only normal form of altered consciousness, Dementia delusion