Thursday, May 16, 2013


 Impairment of the capacity to think with normal
speed and clarity, associated with inattentiveness and disori-
entation. Delirium is a special example of an acute confu-
sional state in which impaired attention and reasoning are
associated with agitation, hallucinations, and in some cases,
tremor and convulsions.

 Inability to remain awake without external
stimulation; often associated with some degree of confusion.

 State in which only vigorous external stimulation
can arouse the patient; once aroused, responses remain
markedly impaired.

 Deep sleep-like state; patient cannot be aroused even
with vigorous or repeated external stimulation.

Causes of change in consciousness
1. With abnormal CT scan
• Hemispheric mass lesions that cross the midline or
impinge upon the brainstem.
• Brainstem lesions that directly affect the reticular forma-
• Subarachnoid hemorrhage.
2. With normal CT scan
• Inflammatory disorders, such as bacterial meningitis and
viral encephalitis.
• Exogenous toxins,such as sedative drugs,alcohols,opioids,
and carbon monoxide.
• Endogenous metabolic insults, such as global hypoxic-
ischemic insults, hypoglycemia, hyperammonemia, and
• Postictal state.
• Selective brainstem ischemia.

Diagnosis of cause of changes in consciousness:
Establishing a differential diagnosis for the cause of a patient’s change in
consciousness requires evaluation of the history preceding the
change,the physical examination,and the effectiveness of initial
empirical therapy.
Categories of cause of changes in consciousness
 Toxic and metabolic (e.g., opiate overdose, alcohol).
 Infectious (e.g.,meningitis,encephalitis,septic shock).
 Cerebrovascular (e.g.,stroke).
 Other (e.g.,seizures,neoplasms).

Role of history in diagnosis of changes in consciousness

  •  Preceding headache suggests meningitis,subarachnoid hemorrhage, or encephalitis.
  •  Preceding intoxication,confusion,or delirium suggests a diffuse process such as meningitis, endogenous metabolic insults, or exogenous toxins.
  •  Sudden onset of coma suggests brain stem infarct or hemorrhage (e.g., subarachnoid hemorrhage).

Role of physical examination in diagnosis of changes in
Localizing signs: Suggest focal lesion. 
> No localizing signs: Suggests encephalopathy as a result of
either an exogenous toxin or an endogenous metabolic
>  Important Structural versus Metabolic causes of COMA
 Asymmetrical or reflex functioning of the motor system indi-
cates a focal mass lesion. Changes in pupillary size and reflexes
are also useful in assessing the cause of coma.
 A unilaterally dilated nonreactive pupil suggests oculomotor
nerve (CN III) compression by an expanding hemispheric
> Pinpoint minimally reactive pupils suggests compromise of
the pontine tegmentum (e.g., in a pontine hemorrhage);
may also be seen in opiate intoxication. Small but reactive
pupils are a feature of many metabolic encephalopathies.
> Minimally reactive pupils in a mid or slightly dilated posi-
tion suggests a midbrain lesion.
> Bilaterally dilated, nonreactive pupils can be seen in cases of
damage to the midbrain tectum or in global ischemic brain
injury. It may also be caused by atropine and similar anti-
cholinergic agents.

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