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Description
A patient was found unresponsive but breathing with blood glucose of 45 mg/dL following insulin overdose. On unsedated examination the following day the patient's eyes were roving with limbs flaccid. The best responsiveness was triple flexion withdrawal of the left leg to deep nail bed pressure. There was a continuous symmetric low amplitude 3–4 Hz pill-rolling type rest tremor of both hands.
To the best of the author's knowledge this is the first report of rest tremor in deep coma. There is one prior case, including video, of a similar tremor in a patient following brain death.1 As in the prior case, the tremor was short lived, lasting <24 hours.
Specific regional vulnerability is seen with hypoxia and various toxins such as organophosphates or manganese. Vulnerabilities may vary by metabolic demand, vascular supply, biochemical milieu or other factors. Hypoxic and hypoglycaemic injury preferentially affect the grey matter. However, hypoglycaemic injury is characterised by thalamic sparing.2 This was seen in the present patient (figure 1). Also notable is sparing of the pallidum, including the internal globus pallidus (GPi), a major output pathway for the basal ganglia.
While in this case selective pallidal sparing was associated with emergent rest tremor, selective pallidal damage may also be associated with emergent rest tremor (eg, manganese or carbon monoxide poisoning). In Parkinson's disease and essential tremor ablation or deep brain stimulation to the thalamus or GPi alleviates tremor. Despite extensive research, the circuitry involved in Parkinsonian rest tremor is poorly understood.3
Learning points
There are structurally specific vulnerabilities to generalised toxic/metabolic brain injury.
Rest tremor can occur despite loss of all voluntary movement in deep coma.
Footnotes
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.