Neurological assessment of coma (pdf)
David E Bateman
J Neurol Neurosurg Psychiatry
2001; 71(suppl I); i13Ði17

mise à jour du 18 avril 2002
N Engl J Med
1994; 330; 21; 1469-1475
 cas cliniques
 Neuropathological Findings in the Brain of Karen Ann Quinlan
The Role of the Thalamus in the Persistent Vegetative State.
Kinney, H. C., J. Korein, et al.
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Karen Ann Quinlan had a cardiopulmonary arrest in 1975 and died 10 years later, having never regained consciousness. Her story prompted a national debate about the appropriateness of life-sustaining treatment in patients who are in a persistent vegetative state and led to the development of medicolegal guidelines for the care of such patients.

Case Report : The clinical history and findings are based on examination of the patient by one of us, interviews with the attending physicians, and a review of all relevant documents, including medical and nursing records. At 21 years of age, Karen Ann Quinlan had a cardiopulmonary arrest after accidentally ingesting a combination of prescription sedatives and alcohol. When she was found, she was unresponsive, apneic, pulseless, and cyanotic with dilated pupils. She received cardiopulmonary resuscitation. In the emergency room, a pulse was present, but she was otherwise unchanged and was placed on a ventilator. Within the first hour after cardiopulmonary arrest, spontaneous respirations and normal vital signs had returned, but the patient remained unresponsive to noxious stimuli and was areflexic. During the first 12 hours, there was sequential improvement, with the development of pinpoint pupils and sluggish reaction to light, upper-extremity flexion, toe inversion, responsivity to pain, gag and cough reflexes, spontaneous movement of all extremities, and finally, opening of the eyes in response to auditory stimuli. Aspiration pneumonia led to a tracheostomy on the second day. Hypoxia occurred transiently, with a low arterial partial pressure of oxygen of 45 mm Hg. During the first week after the arrest, stimulus-induced postural patterns were seen, including flexion and clenching of the hands, plantar flexion and inversion of the feet, turning of the head to the right, yawning, and grunting. With intense stimulation, there was flexion of the upper and lower extremities with marked spastic rigidity, opisthotonos, and upward rolling of the eyes. There was no response to threatening gestures. Oculocephalic and oculovestibular reflexes had returned to normal. All extremities withdrew in response to a pinprick.

During the first six months after the arrest, Quinlan had unequivocal sleep-wake cycles but never showed signs of awareness of her environment or cognitive function. During sleep she rarely triggered the ventilator. Severe contractures developed, and orofacial movements (e.g., grimacing) dominated the arousal responses in association with marked diaphoresis, tachycardia, and tachypnea. Quinlan's movements were never goal-directed but always stereotypical and reproducible with a given stimulus. Although she had the full range of eye movement, her eyes moved randomly with occasional disconjugate components, and she never responded to stimuli with meaningful extraocular movements. Quinlan had sufficient primary motor competence to respond in a meaningful fashion had any cognitive function been intact, which buttressed the clinical diagnosis of a persistent vegetative state, not a locked-in state (i.e., conscious but with severe paralysis, making vocal communication impossible). A brain scan and bilateral carotid and vertebral angiograms were unremarkable. Electroencephalograms showed cortical activity (predominantly low-voltage fast activity [beta]) when the patient was awake. When she appeared to be asleep, there was intermittent low-voltage activity of 3 to 7 Hz , infrequent activity in the alpha range, and occasional slower activity in the delta range. During the first six months after the arrest, the patient became severely cachectic, and her weight stabilized at 32 to 34 kg (down from 52 kg) with hypercaloric feeding. Multiple lung, bladder, and decubitus-ulcer infections were treated.

During the second six months after the arrest, Quinlan began to trigger the ventilator more frequently while asleep, and she was weaned from it over a period of a month, one year after the arrest. Seizures (episodic twitching of the extremities, mouth, and eyes for about 30 seconds) developed and were successfully treated with phenytoin. A computed tomographic scan five years after the arrest revealed cerebral and cerebellar atrophy with generalized dilatation of ventricular and cisternal systems. Fourteen months after the arrest, Quinlan was transferred to a nursing home where she remained in a persistent vegetative state until her death nine years later from overwhelming infection.

This report describes the neuropathologic features of Quinlan's brain.

Methods : The entire brain and spinal cord were systematically sampled for histologic examination. The brain stem and central cerebrum were embedded en bloc and serially sectioned. Three-dimensional computer reconstructions helped visualize the topographic features of the lesions.

Results : Contrary to expectation, the most severe damage was not in the cerebral cortex but in the thalamus, and the brain stem was relatively intact. The neuropathological findings included extensive bilateral thalamic scarring, bilateral cortical scars primarily in the occipital pole and parasagittal parieto-occipital region, and bilateral damage to cerebellar and focal-basal-ganglia regions. The brain stem and basal forebrain and the hypothalamic components of the ascending arousal systems and brain-stem regions critical to cardiac and respiratory control were undamaged. The lesions were consistent with hypoxia-ischemia after the cardiopulmonary arrest.

Conclusions : Although the neuropathological findings in the case of Karen Ann Quinlan were complex, the disproportionately severe damage in the thalamus as compared with the cerebral cortex supports the hypothesis that the thalamus is critical for cognition and awareness and may be less essential for arousal.


There was severe atrophy of the cerebral cortex and underlying white matter in the border zone of the anterior, middle, and posterior cerebral arteries in the posterior frontal lobe (short arrow). The thalamus (long arrow) was severely atrophic bilaterally. (Hematoxylin and eosin and Luxol fast blue.).

The permanent vegetative state : practical guidance on diagnosis and managment
DT Wade, C Johnston BMJ vol 319; 25/09/99
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