Prodromal stage

Kuru typically begins with prodromal symptoms consisting of headache, aching of limbs, and joint pains which can last for several months. Ambulatory stage

Kuru was frequently self-diagnosed by patients at the earliest onset of unsteadiness in standing or walking, or of dysarthria or diplopia. At this stage there may be no objective signs of disease. Gait ataxia, however, worsens and patients develop a broad-based gait, truncal instability, and titubation. A coarse postural tremor is usually present and accentuated by movement; patients characteristically hold their hands together in the midline to suppress this. Standing with feet together reveals clawing of toes to maintain posture. This marked clawing response is regarded as pathognomonic of kuru. Patients often become withdrawn at this stage and occasionally develop a severe reactive depression. Prodromal symptoms tend to disappear. Astasia and gait ataxia worsen and the patient requires a stick for walking. Intention tremor, dysmetria, hypotonia, and dysdiadochokinesis develop. Although eye movements are ataxic and jerky, nystagmus is rarely seen. Strabismus, usually convergent, may occur particularly in children. This strabismus does not appear to be concomitant or paralytic and may fluctuate in both extent and type sometimes disappearing later in the clinical course. Photophobia is common and there may be an abnormal cold sensitivity with shivering and piloerection even in a warm environment. Tendon reflexes are reduced or normal and plantar responses are flexor. Dysarthria usually occurs. As ataxia progresses the patient passes from the first (ambulatory) stage to the second (sedentary) stage. The mean clinical duration of the first stage is around 8 months and correlates closely with total duration. (42>

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