Prof., Dr. :sherif wadie

Reticular activating system (RAS)

 Good Consciousness = Alertness + Awareness

 Diminished alertness = Widespread abnormalities of cerebral hemispheres or reduced activity of reticular activating system (RAS)

 Confusion :  Impaired attention and concentration, manifest disorientation in time, place and person, impersistent thinking, speech and performance, reduced comprehension and capacity to reason  Fluctuate in severity, typically worse at night ‘sundowning’  Perceptual disturbances and misinterpret voices, common objects and actions of other persons  Confusion is also found in dementia (progressive failure of language, memory, and other intellectual functions)

 Delirium : confusion and associated agitation, hallucination, convulsion and tremor  Amnesia : a loss of past memories and to an ability to form new ones, despite alert and normal attentiveness

 Alert : normal awake and responsive state  Drowsiness : state of apparent sleep, briefly arousal with oral command  Lethargic : resembles sleepiness, but not becoming fully alert, slow verbal response and inattentive. Unable to adequately perform simple concentration task (such as counting 20 to 1)

 Somnolent : easily aroused by voice or touch; awakens and follows commands; required stimulation to maintain arousal  Obtunded/Stuporous : arousable only with repeated and painful stimulation; verbal output is unintelligible or nil; some purposeful movement to noxious stimulation  Comatose : no arousal despite vigorous stimulation, no purposeful movement- only posturing, brainstem reflexes often absent

 Dementia  Longstanding nature  Varies little from time to time  Memory problem  Confusional state  Acute  Fluctuate  Clouding of consciousness

Medical or surgical disease  Metabolic disorders  Hepatic  Uremic  Hypo and hypernatremia  Hypercalcemia  Hypo and hyperglycemia  Hypoxia  Hypercapnia

 Infectious illness  Pneumonia  Endocarditis  Urinary tract infection  Peritonitis  Congestive heart failure  Postoperative and posttraumatic states

Drug intoxication  Opiates  Barbiturates  Other sedatives

Diseases of nervous system  Cerebrovascular disease, tumor, abscess  Subdural hematoma  Meningitis  Encephalitis  Cerebral vasculitis  Hypertensive encephalopathy

Alcoholism. Depression. Diabetes. Drug overdose Head injuries Encephalitis Epilepsy Stroke causes of confusional state (5)

 History --- emphasizing the patient’s condition before the onset of confusion  Clinical examination --- focus on  signs of diminished attentiveness, disorientation, and drowsiness and  the presence of localizing neurological signs

 Control underlying medical illness  Quiet the patient and protect him from injury - Discontinue drugs that could possibly be responsible for the acute confusional state : sedating, antianxiety, narcotic, anticholinergic, antispasticity, corticosteroid, L-dopa, metoclopramide, cimetidine, antidepressant, antiarrhythmic, anticonvulsant, antibiotics.

- Haloperidol, quetiapine, risperidone are helpful in calming the agitated and hallucinating patient, but should be used in the lowest effective doses - In alcohol or sedative withdrawal— chlordiazepoxide is the drug of choice. Chloral hydrate, lorazepam, and diazepam are equally effective

Eye opening: Nil 1 To pain (applied to limbs) 2 To voice (including command) 3 Spontaneous (with blinking) 4 Motor response: Nil 1 Arm extension to pain (nail bed pressure) 2 Arm flexion to pain (nail bed pressure) 3 Arm withdrawal from pain (nail bed pressure) 4 Hand localizes pain(supraorbital or chest pressure) 5 Obeys commands 6 Verbal response: NIL 1 Groans (no re-cognizable words) 2 Inappropriate words (including expletives) 3 Confused speech 4 Orientated 5

Glasgow Coma Scale : Eye opening (E)

Glasgow Coma Scale : Motor response (M)

Glasgow Coma Scale : Verbal response (V)

Notes 1. scoring from the best response 2. verbal response will not correct in the condition of aphasia, intubation and facial injury 3. sensory loss may interfere painful stimulation 4. eye opening may be interfered by orbital swelling and 3 rd CN palsy 5. arm movements may be impaired from local trauma or cervical cord lesion GLASGOW COMA SCORE

 History  Circumstances and rapidity with which neurologic symptoms developed  Immediately preceding medical and neurologic symptoms  Use of medications, illicit drugs, or alcohol  Chronic liver, kidney, lung, heart, or other medical disease

 Vital sign  Temperature  Fever  Hypothermia -- <31°C causes coma  Pulse  Respiratory rate and pattern  Blood pressure  Funduscopic examination  Cutaneous lesion

 Observe  Movement : restless, twitching, multifocal myoclonus, asterisks  Decorticate rigidity Suggest severe bilateral damage rostral to midbrain  Decerebrate rigidity Indicate damage to motor tracts in the midbrain or caudal diencephalon

 Level of arousal and elicited movements  Brainstem reflexes  pupils  Ocular movements  respiration

DESCRIPTIONSINTERPRETATION Small, reactiveMetabolic causes Diencephalic lesion Midposition, fixedMid brain lesion large, fixedExtensive brain stem lesion Anoxia Sedative overdose Anticholinergic poisoning or mydriatic eyedrops Pin pointPontine lesion Opiates Unilateral fixed dilatedThird nerve palsy

Doll’s eye maneuver (Oculocephalic reflex) Cold caloric test (Oculovestibular reflex)

ConditionAwake Cerebral dysfunction, brainstem intact Brain stem lesion Doll’s eyes NegativePositive Negative NegativeConditionAwake Cerebral dysfunction, brainstem intact Brain stem lesion Cold calorics Nystagmus, N/V, pain Slow deviation toward water Negative

Respiratory patterns

 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

 Least useful sign because :  Acid-base derangements  Hypoxia  Cardiac influences

 Brain death  Locked-in syndrome  Vegetative state  Frontal lobe disease  Non-convulsive status epilepticus  Psychiatric disorder (catatonia, depression)

 An awake but unresponsive state  Extensive damage in both cerebral hemisphere  Retained respiratory and autonomic functions  Cardiac arrest and head injury are the most common causes.

 Awake patient has no means of producing speech or volitional limb, face and pharyngeal movements  Vertical eye movement and lid elevation remain unimpaired  Infarction or hemorrhage of the ventral pons

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

 CBC  FBS  BUN, Creatinine  Electrolyte, calcium  LFT  Drug screen, toxicology screen

 EKG  CT or MRI brain  CSF exam  EEG

 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 3 rd day, no papillary light reflex or GCS < 5 is associated with poor prognosis

 Central transtentorial herniation

Uncal transtentorial herniation  Uncal transtentorial herniation Brain Herniation

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