Coma
RELATED DISORDERS OF CONSCIOUSNESS
= suspension of consciousness→ a state of continuous awareness of one’ self and one’
environment
Consciousness depend by the integrity of reticular activating system of the upper
brainstem = paramedian regions of the upper (rostral) pontine and midbrain tegmentum
+ thalamic nuclei (PM, parafascicular, medial portion of centromedian and intralaminar)
↓
Receive collaterals of the direct spinothalamic pathways
→ Whole cerebral cortex
↓
Modulates the incoming information via corticofugal projections to the reticular formation
Coma-producing alterations in the brain are of two main types
I one clearly morphologic
a) Discrete paramedial lesions in the upper brainstem and lower diencephalon
b) Widespread bilateral damage to the cortex and subcortical white matter (traumatic
damage, bilateral infarcts, hemorrhages, encephalitis, hypoxia)
II submicroscopic →suppression of neuronal activity =metabolic, drugs , toxin
Mass lesion cause coma
a) Direct extension of the lesion into the diencephalon and midbrain
b) Lateral displacement of deep central structures, often with temporal lobe herniation →
compression, ischemia and secondary hemorrhages in the midbrain and subthalamic
region →central syndrome with downward displacement and bilateral compression of the
upper brainstem !→ rostral-caudal deterioration of brainstem function →apathy,
confusion, drowsiness , coma
1
,Miotic pupils
→uncal syndrome with unilateral displacement and uncal gyrus herniation
→the Kernohan – Woltman sign = compression of the opposite cerebral peduncle »
Babinski sign and hemiparesis controlateral to the original hemiparesis
! Differs mainly in that drowsiness in the early stages is accompanied or preceded by
unilateral pupillary dilatatation (most often on the side of the mass)
3-5 mm →drowsiness
5-8 mm →stupor
8-9 mm →coma
Diagnosis
A. Positive diagnosis –
1) Anamnesis – antecedents, circumstances in which the person was found, use of
medications
2) Clinical exam - * general physical exam
* nuchal rigidity
* fundoscopy
**neurologic
3) Laboratory studies and imaging
B. Differential diagnosis
2
, C. Causes of coma= Aethiological diagnose
! Coma is not a disease per se but is always a symptomatic expression of an underlying
disease.
When the comatose patient is first seen → quickly make certain →airway is clear
No bleeding
IV access
Cervical
stabilisation
Alterations in vital signs
A. Temperature - fever = Intoxication with anticholinergic
hypothermia = Alcohol,barbiturate, myxedema
B . Respiration Rate – slow breathing = Barbiturate, opiate
rapid = Diabetic and uremic acidosis (Kussmaul respiration)
C. Pulse Rate – slow = Cushing fen.
D. Blood Pressure – HTA - Increased intracranial pressure
- hTA !!!
E. Inspection of the Skin
F. Odor of the Breath
Neurologic Examination
A. Posture of the limbs and body
B. Presence or absence of spontaneous movements
- Seizures
- Multifocal myoclonus →metabolic disorder (uremia, anoxia, drug intoxication)
- Decorticate rigidity →lesions at a more rostral level of the nervous system – in the
cerebral white matter or internal capsule and thalamus
3
RELATED DISORDERS OF CONSCIOUSNESS
= suspension of consciousness→ a state of continuous awareness of one’ self and one’
environment
Consciousness depend by the integrity of reticular activating system of the upper
brainstem = paramedian regions of the upper (rostral) pontine and midbrain tegmentum
+ thalamic nuclei (PM, parafascicular, medial portion of centromedian and intralaminar)
↓
Receive collaterals of the direct spinothalamic pathways
→ Whole cerebral cortex
↓
Modulates the incoming information via corticofugal projections to the reticular formation
Coma-producing alterations in the brain are of two main types
I one clearly morphologic
a) Discrete paramedial lesions in the upper brainstem and lower diencephalon
b) Widespread bilateral damage to the cortex and subcortical white matter (traumatic
damage, bilateral infarcts, hemorrhages, encephalitis, hypoxia)
II submicroscopic →suppression of neuronal activity =metabolic, drugs , toxin
Mass lesion cause coma
a) Direct extension of the lesion into the diencephalon and midbrain
b) Lateral displacement of deep central structures, often with temporal lobe herniation →
compression, ischemia and secondary hemorrhages in the midbrain and subthalamic
region →central syndrome with downward displacement and bilateral compression of the
upper brainstem !→ rostral-caudal deterioration of brainstem function →apathy,
confusion, drowsiness , coma
1
,Miotic pupils
→uncal syndrome with unilateral displacement and uncal gyrus herniation
→the Kernohan – Woltman sign = compression of the opposite cerebral peduncle »
Babinski sign and hemiparesis controlateral to the original hemiparesis
! Differs mainly in that drowsiness in the early stages is accompanied or preceded by
unilateral pupillary dilatatation (most often on the side of the mass)
3-5 mm →drowsiness
5-8 mm →stupor
8-9 mm →coma
Diagnosis
A. Positive diagnosis –
1) Anamnesis – antecedents, circumstances in which the person was found, use of
medications
2) Clinical exam - * general physical exam
* nuchal rigidity
* fundoscopy
**neurologic
3) Laboratory studies and imaging
B. Differential diagnosis
2
, C. Causes of coma= Aethiological diagnose
! Coma is not a disease per se but is always a symptomatic expression of an underlying
disease.
When the comatose patient is first seen → quickly make certain →airway is clear
No bleeding
IV access
Cervical
stabilisation
Alterations in vital signs
A. Temperature - fever = Intoxication with anticholinergic
hypothermia = Alcohol,barbiturate, myxedema
B . Respiration Rate – slow breathing = Barbiturate, opiate
rapid = Diabetic and uremic acidosis (Kussmaul respiration)
C. Pulse Rate – slow = Cushing fen.
D. Blood Pressure – HTA - Increased intracranial pressure
- hTA !!!
E. Inspection of the Skin
F. Odor of the Breath
Neurologic Examination
A. Posture of the limbs and body
B. Presence or absence of spontaneous movements
- Seizures
- Multifocal myoclonus →metabolic disorder (uremia, anoxia, drug intoxication)
- Decorticate rigidity →lesions at a more rostral level of the nervous system – in the
cerebral white matter or internal capsule and thalamus
3
