1. Coma is defined as a deep sleep-like state from which the patient cannot be aroused. It can be caused by lesions that damage the reticular activating system in the upper midbrain or its projections, or destruction of a large portion of the cerebral hemisphere. 2. The causes of coma include cerebral mass lesions, metabolic disorders, toxic or drug-induced states, and widespread damage to the cerebral hemispheres. 3. Evaluation of a comatose patient involves assessing their history, performing a neurological examination including assessment of eye movements and motor responses, and ordering investigations such as CT/MRI, EEG, and CSF examination.

1. ANOOP K R

2.  Mental and behavioural state of reduced
comprehension , coherence and capacity to
reason.

3.  Using a well valid CAM, the diagnosis of
delirium is made if
 1.acute onset and fluctuating cause
 2.inattention accompanied by either
disorganized thinking
 3.An altered level of consciousness.
 Other features include alteration of sleep-
wake cycle , thought disturbances ,
autonomic instability,changes in effect.

5.  It is difficult to obtain history from delirious
patient- so collateral history from spouse.
 Three imp: baseline cognitive function, time
course of present illness , current medication.
 Premorbid cognitive function-collateral
sources like OP record check for h/o
unrecognised underlying neurological
disorder.
 Time course –corelate with treatable
etiologies –medication,systemic infection

6.  Screen for symptoms of organic failure or
systemic infection –in elderly.
 In young – illicit drug use, alcoholism , toxin
exposure
 Other associated features like depression

7.  GPE: Signs of infection-fever , tachycardia,
pulmonary consolidation, heart murmur ,stiff
neck.
 Fluid status:dehydration,fluid overload +
hypoxemia
 Look for jaundice(hepatic encephalopathy) ,
cyanosis(hypoxemia),needle track

8.  Altered level of consciousness-hyperarousal –
coma
 Attentional deficit- classical neuropsyciatric
hallmark
 Tested by tangential speech,fragmentary flow
of ideas,inability to follow complex
commands
 MMSE(mini mental state examination)-
orientation,language,visualspatial skills.

11.  Reminder includes identifying new focal
neurological deficit.
 Screen for other neurodegenerative
conditions-parkinsonism,alzheimier’s disease
,PSP.
 Multifocal myoclonus or asterixias on motor
system non specific-indicates metabolic or
toxic etiology.

15.  Definition :deep sleep like state from which the patient
cannot be aroused.
 Misinterpretations of coma
 1.vegitative state:awake-appearing but non-responsive
state in patient who has emerged from coma.
 2.minimally concious state:patient has rudimentory vocal
or motor behaviour, often spontaneous
 3.akinetic mutism;syndrome misinterpreted as coma
where patient is awake can think but virtually immobile
and mute
 4.catatonia:hypermobile and mute syndrome
 5.locked in syndrome:pseudocoma in which awake patient
has no means of producing speech or violationaty
movement but retains voluntary eye movements

16. LOCALIZING SIGN NO LOCALIZING SIGN
INFRATENTORIAL
NO STIFF NECK
SUPRATENTORIAL
- CVD
- TUMOUR
- ABSCESS
STRUCTURAL DAMAGE FUNCTIONAL NEURONAL
DEPRESSION
- HYPOXIA
-CARDIAC
ARREST
- ENCEPHALITIS
- HEPATIC
- URAEMIC
- POST ICTAL STATE
- FLUID ELECTROLYTE IMBALANCE
- DRUGS
STIFF NECK
- SAH
- MENINGITIS

18.  The causes of coma include
 1. lesions that damage RAAS in upper
midbrain or its projection
 2.destruction of large portion of cerebral
hemisphere.
 3. suppression of reticulocerebral functions
by drugs,toxins,or metabolic derrangement.

19.  1.coma due to cerebral mass lesion and
herniation
 2.coma due to metabolic disorders
 3.epileplic coma
 4.toxic coma
 5.coma due to widespread damage to
cerebral hemisphere.

21.  HISTORY
 1. circumstances and rapidity with which
neurologic symptoms developed
 2.antecedal
symptoms(confusion,weakness,headache,feve
r,seizure,dizziness,double vision)
 3.use of medication,drug,alcohol
 4.chronic lung,kidney,liver,heart or other
medical disease

22.  GPE:fever-sys.infctn,bacterial
meningitis,encephalitis
 Hypothermia-alcohol,barbiturate,sedative
 Tachypnea-systemic
acidosis/pneumonia,infiltration of brain stem
 Hypertension-hyp.encepalopathy,cerebral
haemorrhage,head injury
 Hypotension-mi,alcoho;,barbiturate
 Fundoscopy-subarachinoid
 haemorrhage,incrsd ICT
 Cut.petechie-TTP

23.  Lack of restless movemnts to one side
/outturned leg-hemiplegia
 Intermittent twiching of foot,finger,facies-seizure
 Multifocal myoclonus-
metabolic,lithium/haloperidol
 b/l asterixis-metabolic encepalopathy
 Decorticate-flxtn of elbow & wrist ,supination of
arm-b/l midbrain rostral damage
 Decerebrate-extension of elbow& wrist with
pronation-damage to motor tract ,caudal
diencephalon

25.  Observe
– Movement : restless, twitching, multifocal
myoclonus, asterixis
– Decorticate rigidity
Suggest severe bilateral damage rostral to
midbrain
– Decerebrate rigidity
Indicate damage to motor tracts in the midbrain or
caudal diencephalon

26.  Level of arousal:posturing in response to noxious
stumili-damage to corticospinal system
 BRAINSTEM REFLEX:localization of coma
 Pupilary signs:enlarged and poorly reactive
pupil>6mm-comression or steching of 3rd nerve
due to cerebral mass above
 b/l dilated & unreactive-severe midbrain lesion
 U.l miosis large cerebral hemmmorhage
 Reactive and small pupil-metabolic
encepalopathy
 Pin point pupil-narcotic or barbiurate
overdoe,pontine hemmorhage

27.  OCCULAR MOVEMENTS
 Spontaneous eye movement-horizontal
roving
 Conjugate horizontal deviation –pons on
opp.side ,cerebral on same side
 Occular bobbing-b/l pontinr
 Occular dipping-cortial anoxic damage
 Occulocephalic reflex-movemnts in direction
opposite to head movement dolls eye-
presentlesion in cerebral hemisphere
 Absent-brainstemlesion

29.  Ooculovestibular response-loss of conjucate
movement-brain stem lesion
 Corneal reflex intact-intact pons
 RESPIRATORY PATTERN-chyne stroke’s

30. Cold caloric test
(Oculovestibular
reflex)

32.  Cheyne-Stokes respiration : bilateral cortical
or bilateral thalamic lesions, metabolic
disturbances, incipient transtentorial
herniation
 Hyperventilation : midbrain or pons lesions
 Apneusis : lateral tegmentum of lower half
of pons
 Cluster : lower pontine or high medullary
lesions
 Ataxic : dorsomedial medulla lesion

33.  LAB INVESTIGATIONS-CT,MRI,EEG,CSF
examination
 ABG,electrolytes,tox screen

35.  Recovery from coma depends primarily on the
causes, rather than on the depth of coma
 Intoxication and metabolic causes carry the best
prognosis
 Coma from traumatic head injury far better than
those with coma from other structural causes
 Coma from global hypoxic-ischemic carries least
favorable prognosis
 At 3rd day, no papillary light reflex or GCS < 5 is
associated with poor prognosis

36.  Central
transtentorial
herniation

37. Uncal
transtentorial
herniation

38.  Intubation and hyperventilation (PCO2
25-30
mmHg)
 Mannitol (0.5-1 gm/kg body weight or 20%
mannitol 200 cc. infusion 10-20 minutes repeat
every 4 hours if necessary
 Furosemide 20-40 mg IV
 Dexamethasone 4-10 mg IV q 6 hours
decrease perilesional vasogenic cerebral
edema. Active at 24-48 hours.
 Consult surgery