Написане мною нижче – це по суті об’єднані та дещо скорочені дві статті:

Третю, варто читати в оригіналі – https://litfl.com/examination-of-the-unconscious-patient/

NEUROANATOMICAL BASIS OF COMA

Coma is caused by:

  • diffuse bilateral hemisphere damage
  • failure of the ascending reticular activating system
  • both
  • Bilateral thalamic and hypothalamic lesions ( by interrupting activation of the cortex mediated through these structures)

Lesions below the level of the pons do not normally result in coma.

Drugs and metabolic disease produce coma by a depression of both cortex and ascending reticular activating system function.

Sites and causes of coma

The approach to clinical evaluation is used to categorise coma into:

  • Coma without focal signs or meningism – most common, anoxic-ischaemic, metabolic, toxic, and drug induced insults, infections, and post ictal states.
  • Coma without focal signs with meningism – subarachnoid haemorrhage, meningitis, and meningoencephalitis.
  • Coma with focal signs – intracranial haemorrhage, infarction, tumour or abscess.

ASSESSMENT

The neurologist has to determine:

  • where is the lesion responsible for coma?
  • what is its nature?
  • what is it doing?

Clinico-anatomical correlation in coma:

  • Bilateral hemisphere damage/dysfunction:
    – symmetrical signs (tone and flexor or extensor response to pain)
    – may have fits or myoclonus
    – normal brain stem reflexes
    – normal oculocephalic response (OCR) and normal calorics
    – normal pupils
  • Supratentorial mass lesion with secondary brain stem compression
    – ipsilateral third nerve palsy
    – contralateral hemiplegia
  • Brain stem lesion
    – early eye movement disorder: abnormal OCR or calorics
    – asymmetrical motor responses
  • Toxic/metabolic
    –normal pupils: single most important criterion (except opiate poisoning)
    – ocular motility: rove randomly in mild coma and come to rest in primary position with deepening coma
    – absent OCR and calorics
    – decorticate and decerebrate rigidity or flaccidity
    – multifocal myoclonus

I. Depth of Coma

1) Glasgo Coma Scale

Assessment technique – https://geekymedics.com/glasgow-coma-scale-gcs/

II. Brainstem function

1) Respiration pattern

  • a) Cheyne-Stokes respiration – a pattern of alternating hyperventilation and hypoventilation seen with bilateral cerebral dysfunction or basal ganglia lesions;
  • b) Central neurogenic hyperventilation, produces rapid respiratory rate of up to 40-70/minute and is seen with midbrain dysfunction;
  • c) Apneustic breathing refers to slow breathing with a prolonged pause after inspiration. This occurs with pontine dysfunction;
  • d) Cluster breathing results in brief burst of breaths followed by silence; pontine
  • e) Ataxic (Biot’s ) respirations refer to irregular respiratory frequency and amplitude and indicates medullary dysfunction with impending respiratory arrest.

The above respiratory patterns may occur in a step-wise pattern in transtentorial herniation.

Toxic or metabolic coma – Kussmaul’s breathing.

2) Pulse and Blood Pressure

Hypotension – medullary depression (ex: severe barbiturate intoxication) or contributing factor to coma.

Hyperthension – brain stem dysfunction or reflects the cause.

!!! Cushing’s triad (ICP signs):
hyperthension+ bradicardia + apnoe = impending brain herniation

3) Pupillary Reactions

Lesions above the thalamus and below the pons preserve pupillary reactions.

Small but reactive -> metabolic coma.

Unilateral/bilateral fixed pupils -> uncal herniation (due to III nerve compression)

4) Eye movements

Spontaneous movements and eyes deviation

Disconjugate eye movements imply sixth or third nerve or intrinsic brainstem lesions.

Roving eye movements (slow, conjugate, horizontal) – intact 3rd nerve nuclei and connections = toxic, metabolic or bilateral hemisphere cause for coma.

Sustained lateral conjugate deviation of the eyes -> lesion of ipsilateral cerebral hemisphere (eyes to lesion) or contralateral pons. 

Irritative or epileptic foci -> contralateral conjugate eye deviation, with or without other obvious manifestations of seizures. Consider EEG for status epilepticus.

Upward and downward – poor localising sign.

Skew deviation occurs with posterior fossa lesions.

Reflex movements

Normal reflex eye movements -> the pontomedullary junction to the level of the ocular motor nucleus in the mid brain is intact.

1) Oculocephalic reflex (doll’s eyes) – if stable neck. (3, 4, 6, 8 CNs + MLF integrity)

Intact oculocephalic reflex indicates basic functioning of the medulla (8th CN), pons (4 and 6th CN) and midbrain (3rd CN).Proceed to calorics only if doll’s eyes absent.

2) Vestibulo-ocular reflex (cold-calorics) – check the tympanic membrane first.

Infusion of 50ml of ice-cold water into external auditory meatus.

Both indicate brain stem dysfunction.

Caloric is more sensitive.

5) Corneal Reflex

Tests CNs – V1 + VII (pons) Should result in bilateral eye blinking.

6) Motor examination

Resting position and spontaneous movements should be documented.

Eyes and head are deviated to the side opposite hemiparesis -> hemisphere lesion
Deviation to the side of hemiparesis -> a pontine lesion.

Posturing:

  • Decorticate – occur with lesions higher in the neuraxis, at the midbrain or above.
  • Decerebrate – occur with more severe lesions extending lower down in the brainstem.
  • Triple flexion – does not require brainstem function and depends only on spinal cord circuitry.

It is important to distinguish these reflexes from purposeful withdrawal. You can make this distinction by pinching the skin on the extensor and flexor sides of the limb and noting the direction of movement.

Ex: Purposeful withdrawal always away from painful stimulus. In flexor posturing the arm flexes even when the flexor side of the arm is pinched.

III. Assessment of focal findings

  •  unilateral loss of motor function
  • conjugate eye deviation
  • opthalmoplegia or pupillary asymmetries
  • unilateral hyperreflexia or tone change
  • aphasia
  • unilateral jerking movements

Acute structural damage above the brain stem results in a flaccidity of muscle tone and is asymmetric in comparison to metabolic disorders where such findings are usually symmetrical.

Unilateral decerebrate or decorticate postures can be seen and are an indication of a unilateral lesion. This asymmetry has some localising value.

Motor response to pain. The symmetry or asymmetry of the motor response can assist localisation. (A) Left hemisphere lesion. The two figures illustrate localisation of pain with the left hand and flexion (left hand figure) or extension (right hand figure) on the right. (B) Subcortical: unilateral left sided lesion exerting a variable contralateral effect. The figures illustrate flexion to pain with the left hand with either extension (right hand figure) or flexion with the right and hyperextension in both lower limbs. (C) Midbrain upper pontine: a bilateral upper and lower limb extension response. (D) Lower pontine/medullary: a bilateral extensor upper limb posture with either flaccidity or minimal diminished flexor response in lower limbs.

Seizures in coma:

  • Myoclonic jerking – anoxic/ischaemic encephalopathy and other toxic or metabolic disorders.

Sources:

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