Sensory features of variant Creutzfeldt-Jakob disease

Abstract

Sensory symptoms are a prominent feature of vCJD, occurring in nearly two thirds of cases. They may help distinguish variant from sporadic CJD. They are likely to be of thalamic origin but the recognised MRI changes in vCJD do not correlate with the presence or absence of sensory symptoms. Neuropathological changes in the thalamus, however, show marked astrocytosis and neuronal loss.

The therapeutic potential of interleukin-10 in neuroimmune diseases

“…The common features of NP involve sensory disturbances including spontaneous pain, increased sensitivity to painful stimuli (hyperalgesia), and painful sensitivity to innocuous stimuli (allodynia) (Jensen et al, 2007; Macleod et al, 2002; Rowbotham and Fields, 1996). NP generally remains at least partially refractory to currently available analgesics, and frontline opioid medications have been shown to exacerbate pain and inflammation with chronic use (Hansen et al, 2005; Hutchinson et al, 2007; Salengros et al, 2010; Trevino et al, 2013; van Gulik et al, 2012; Watkins et al, 2009).…”

First hundred cases of variant Creutzfeldt-Jakob disease: retrospective case note review of early psychiatric and neurological features

“…Between a median of four and six months common neurological features included gait disturbance, often in the form of minor unsteadiness, and dysarthria. Paraesthesia and numbness in a similar distribution to and often associated with pain also occurred at a median of 4-6 months and affected nearly half of the patients 7. The combination of a psychiatric disorder with affective or psychotic features and persistent pain, dysarthria, gait ataxia, or sensory symptoms should at least raise the suspicion of variant Creutzfeldt-Jakob disease, particularly if this is combined with any suggestion of cognitive impairment.…”

Mouse Behavioural Studies and What They Can Teach Us about Prion Diseases

“…It receives afferents from spinal pathways to the ventroposterior nucleus (touch, pain, movement, temperature), and cerebellothalamic tracts from the deep cerebellar dentate nucleus to the ventral anterior and ventrolateral thalamus. Thus, dysfunction in thalamic areas could underlie positive and negative sensory symptoms such as paraesthesia, pain or numbness that are often seen in vCJD and other prion diseases 49 . Since severe deficits, such as tremor and ataxia, are caused by lesions to the dentate nucleus, the loss of its projection areas in the thalamus may also have a role in the motor coordination problems ultimately experienced by most patients with prion diseases.…”