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COMA. CONSCIOUSNESS : state of patient’s awareness of self and environment & his responsiveness to external stimuli and inner need IT HAS TWO DIMENSIONS. arousal. cognition. Primary function of deep brainstem and medial thalamic nuclei.

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  1. COMA

  2. CONSCIOUSNESS:state of patient’s awareness of self and environment & his responsiveness to external stimuli and inner need IT HAS TWO DIMENSIONS arousal cognition Primary function of deep brainstem and medial thalamic nuclei Requires an intact cerebral cortex and major sub cortical structures

  3. COMA : State of reduced alertness and responsiveness represent a continuum that in its severest form is called coma , a deep sleep like state from which patient cannot be aroused . Coma among the most common problems in medicine 3 % all admissions from emergency Most common : alcoholism , CVA , cerebral trauma

  4. CONDITION WHICH SIMULATE COMA : persistent vegetative state abulia akinetic mutism catatonia locked in state ( pseudocoma )

  5. RETICULAR FORMATION AND RAS Reticular formation – loosly grouped aggregation of neurons in UPPER BRAINSTEM & MEDIAL THALAMUS In brain stem – paramedian regions of the upper ( rostral ) pontine & midbrain tegmentum In thalamus – posterior paramedian , para follicular , medial portions of Centro median & adjacent intralaminar nuclei Afferent from – spinothalamic , auditiry , visual , trigeminal thalamic pathways

  6. ARAS : System of fibers arise from brainstem reticular formation project rostrally to cortex via thalamic relay nuclei (thalamocortical fibers ) tonic influence on the entire cerebral cortex maintain cerebral cortex in a state of wakeful consciousness anatomical proximity of the structures which control pupillary function & eye movement STIMULATE RAS – AROUSAL DESTRUCTION – COMA Hypothalamus also important for consciousness

  7. ARAS

  8. COMA 1. MORPHOLOGICAL discrete lesions in the upper brainstem or lower diencephalons either primary or secondary to compression 2. METABOLIC widespread changes throughout the hemispheres suppression of neuronal activity Unilateral destructive lesions of hemispheres such as infarct , hemorrhage does not cause coma unless they create some degree of mass effect ( edema ) – compression of brainstem coma

  9. THREE TYPES OF MORPHOLOGICAL LESIONS – COMA • Mass lesion – chiefly tumor , abscess , massive infarct , ICH , EDH , SDH • much of the cerebrum intact • coma by lateral displacement of deep cerebral structures & uncal herniation ( damage to the midbrain & subthalamic RAS ) or direct involvement of the diencephalon & midbrain

  10. 2. DESTRUCTIVE LESIONS in thalamus & in midbrain ( direct damage to RAS ) 3. Widespread damage to cortex and cerebral white matter coma by interruption of thalamo cortical fibers & possible associated damage to thalamus e.g head trauma , bilateral infarct , meningitis , encephalitis

  11. BRAIN HERNIATION DEF: dislocation of the portion of the cerebral or cerebellar hemispheres from its normal position to adjacent compartments. TRANSFALCINE – across the falx TRANSTENTORIAL – through the tentorial apertures UNCAL CEREBELLAR Named by the structures displaced PLUM & POSNER – TRANSTENTORIAL SUBDIVIDED - CENTRAL & UNCAL HERNIATION

  12. Occulomotor nerve PCA TENTORIUM

  13. Sub falcine , uncal & central herniations caused by unilateral, large , destructive , space occupying lesions of the cerebrum – like hemorrhage , tumor , abscess,infarction with cerebral edema • SUBFALCINE HERNIATION : • due to lateral shift across intra cranial cavity • force the cingulate gyrus under the falx • compress & displace internal cerebral vein • also compresses the ipsilateral ACA – ischemia ,congestion , edema • enhance the expanding mass

  14. TRANSTENTORIAL HERNIATION : Two types – central & uncal CENTRAL : Sequential compression of structures from diencephalon – midbrain – pons – medulla ( ROSTROCAUDAL DIRECTION ) – COMA C/ F depends on the structure compressed


  16. UNCAL HERNIATION Lateral compression of the brainstem Herniations of the medial temporal lobe ( UNCUS) into the tentorial opening first manifestation – drowsiness & dilatation of ipsilateral pupil ( 3rd nerve compression, HUTCHINSON PUPIL ) , Later opthalmoplegia some times small pupil , rarely opposite pupil will dilate compression of controlateral cerebral peduncle – hemiparesis ipsilateral to lesion ( KERNOHAN- WOLTMAN PHENOMENON)

  17. Lareral flattening of midbrain & zones of necrosis , secondary hemorrhages in tegmentum , base of subthalamus , midbrain , upper pons (DURET HEMORRHAGES) Unilateral or bilateral occipital hemorrhage – Compression of PCA Increased ICT , HYDROCEPHALUS – flattening of aqueduct , 3rd ventricle block ,, block at peri mesencephalic cisterns





  22. EXTRACEREBRAL LESIONS neoplasms infections hematomas acute head injuries Rarely coma as presentation

  23. NEOPLASMS : Rarely produce problems in diagnosis of coma Most meningiomas , neuromas , pituitory adenomas ,lymphomas – produce FND , headache , sensory , motor , cranial nerve , endocrine changes before they produce coma Lymphomas & metastatic carcinoma in subdural space grow over cerebral convexities & produce motor & other symptoms like SDH RARELY pituitary tumor – coma as a presenting feature

  24. CLOSED HEAD TRAUMA Blunt injury to the cranium extra cerebral , intracerebral & brainstem lesions CAUSES OF COMA IN HEAD INJURY Concussion , Contusion ,Diffuse axonal injury Hematomas – Acute SDH , EDH , ICH Primary brainstem hemorrhage Delayed post traumatic ICH Delayed non hemorrhagic encephalopathy following mild head injury

  25. MECHANISM OF LOC IN HEAD INJURY • Widespread dysfunction of cerebral hemispheres & brainstem or both • Shearing forces disrupt the axons in the white matter and brainstem • Rapidly fatal cases – damage to the blood vessel – diffuse hemorrhages • Cerebral ischemia – contusion , vasomotor paralysis , ICT , Arterial hypotension • EDH , SDH – Uncal herniation or central herniation

  26. ICH (POST TRAUMATIC) ACUTE 2 % of all serious head injury ICH is present in ½ of all fatal cases. Rapidly increase in ICP and death. DELAYED Follow episodes of mild or moderate head injury Delayed upto 4 months Mechnism : not known

  27. EDH : locations frontal lateral or occipital More rapid , more dangerous Bleeding from arteries or veins or both Lateral – most common Due to laceration of middle meningeal artery or vein Enlarge rapidly – coma – death Act as a mass lesion – uncal herniation LUCID INTERVEL +

  28. SDH: acute , sub acute , chronic complication of head injury

  29. SUBDURAL EMPYEMA Rare but important cause of coma Usually a complication of otorhinological disease May follow acute meningitis , rupture of intracerebral abscess , complicate penetrating wound , a surgical procedure Most common area – dorsolateral surface of hemispheres extending from frontal pole M.O. COMA: 1. Act as a supratendorial mass 2. infection involving adjacent brain or impair metabolsm

  30. SAH : acute onset of coma without focal neurological signs INFECTIONS meningitis , encephalitis , cerebral malaria

  31. INTRACEREBRAL LESIONS Neoplasms , hemorrhage , infarction, Abscesses Usually Coma as a late manifestation Easily to localize Usually produce FND before causing coma EXCEPT frontal lobe & intraventricular mass – even widespread anatomical lesion – no focal signs in advances of confusion or coma

  32. CEREBROVASCULAR ACCIDENTS Cerebral hemorrhage , large cerebral infarct – act as expanding mass – diencephalic compression , transtendorial herniation – coma Bilateral thalamic , hypothalamic infarcts– coma

  33. CEREBRAL HEMORRHAGE Most common cause of coma – in supratendorial area ¼ of all cerebral hemorrhage – coma at the onset Coma with in mts or hours of onset of illness Rupture of a blood vessel – usually arteries , leakage from or rupture of aneurysm at the base of the brain , AVM BLEED or microaneurysm bleed , hemorrhage in to asymptomatic primary or secondary tumor.

  34. Spontaneous cerebral hemorrhage -- parenchymal or deep in hemisphere – structures in and around internal capsule especially putamen and thalamus Evolution abrupt 1/3 Smooth 2/3 COMA Causes of coma edema , expanding hemorrhages diencephalic compression , uncal herniation

  35. LOC depends on the size & location of hematoma COMA – poor outcome Most thalamic bleeds extend into ventricular system -- poor prognosis

  36. CEREBRAL INFARCTION Coma seldom as the initial sign in uncomplicated cerebral hemispherical infarct ICA or MCA or MCA + ACA territory infarction can cause coma ( large infarcts ) Coma at the onset associated with systemic hypotension due to MI , arrthymias , acute pulmonary embolism . Uncomplicated infarct » COMA Hyponatremia cerebral edema , pneumonia Transtendorial herniation Transtendorial herniation

  37. CEREBRAL EMBOLISM Coma uncommonly associated with onset of embolism Even infarcts limited to one cerebral hemisphere - COMA COMA after hemispherical embolism – very large infarct affects the opposite hemisphere ( DIASCHISIS) or diencephalon Embolism to both sides of brain – I.E , RHD Silent infarcts in the opposite brain

  38. BILATERAL THALAMIC INFARCTION Rare Infarction involving medial portions of thalamus

  39. CEREBRAL VENOUS & VENOUS SINUS THROMBOSIS Occlusion of cerebral veins or cerebral venous sinuses Causes : Manifest as headache ,, seizures , FND , coma , venous infarcts with or with out hemorrhage + signs of local infection Most common in SSS Severe neurological illness if it involves posterior portion of SSS & it is abrupt onset COMA – due to increase in ICT

  40. INTRA CEREBRAL TUMORS Primary and secondary tumors Uncommon cause , diagnosed before the onset of coma Mechanism of coma : 1. seizures – post ictal coma 2. bleeding in to the neoplasm 3. enlarge progressively swelling & displacement of brain Central or uncal herniation & coma

  41. 4. Lateral and 3rd ventricular tumors suddenly obstructs the ventricular flow & acute ventricular HT Sudden downward displacement of the brainstem recurrent attacks of loc Infiltrate and destroy the RAS in thalamus and hypothalamus – COMA

  42. PITUTITARY APOPLEXY Pituitary apoplexy – sudden enlargement due to infarction or hemorrhage May be a presenting feature or it can occur in pts with known pituitary tumorduring radiotherapy , pregnancy , DIC . Infarction : tumor growth outgrew bloodsupply compression and distortion of blood supply C /F : headache , visual loss , diplopia

  43. Typical pt in stupor or coma with bilateral 3rd & 6th cranial nerve palsies without other FND , Stiff neck , normal pupillary reflex or sluggish Rarely hemiplegia or ataxia Mech of COMA :not clear 1. direct compression of brain stem or diencephalon – may cause coma 2. Sudden release of blood and noxious substances released into suprasellar cistern associated with ICT – COMA

  44. SUB TENTORIAL LESIONS CAUSING COMA PATHOLOGY Two types of lesions – coma 1. Lesion within the brainstem – destroy the Para median midbrain , pontine reticular formation & associated structures 2.Located outside the brain stem that compress the brainstem and RAS

  45. BRAINSTEM DESTRUCTION MECHANISM : 1.Directly invading the brainstem central core 2.Impairing its blood supply – ischemia , necrosis or hemorrhage Most common pathology : stroke Others demyelination , neoplasm , granuloma , abscess , head injury

  46. BRAINSTEM COMPRESSION : Lesions adjacent but outside the brainstem – coma MECHANISM : 1. Direct pressure on the tegmentum of pons and midbrain 2. up ward herniation of the superior vermis through the tentorial notch – compress brainstem and diencephalon 3. Downward herniation of the cerebellar tonsils through foramen magnum – compress and displacing the medulla DEPENDING ON THE SIZE & LOCATION OF THE LESION ANY OF THESE OR ALL MAY CAUSE COMA

  47. Large lesions or rapidly developing lesion – rapid onset of coma e.g cerebellar hematoma Slowly growing lesions – attain large size before causing coma e.g brainstem glioma

  48. INDIVIDUAL LESIONS CAUSING COMA VASCULAR Basilar artery occlusion with midbrain and pontine infarction ( HT, Atherosclerosis , valvular heart disease ) embolism or thrombosis 50 % basilar artery occlusion – coma Coma- abrubt or within few hrs Illness maximal in onset Vertebral artery occlusion Cranial arteritis of vertebral arteries

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