Charcot's arthropathy secondary to herpetic encephalitis sequelae: an unusual presentation.

Neuropathic arthropathy (Charcot's arthropathy) is a progressive articular disease associated with a reduced sensorial and protector proprioceptive reflex. Its etiology includes many different conditions such as syringomyelia, traumatic lesion causing medullary deformity, spina bifida, diabetic neuropathy, leprosy neuropathy, neurofibromatosis, amyloid neuropathy, alcohol, and repetitive injection of hydrocortisone into joints, among others. However, the relationship between Charcot's arthropathy and herpetic encephalitis has not yet been described. Herpes encephalitis causes acute and chronic diseases of the peripheral or central nervous system. It can manifest as subacute encephalitis, recurrent meningitis, or myelitis. It can also resemble psychiatric syndromes, diplopia, sensory changes in the face and limbs, personality changes, frontal dysexecutive syndrome, stiff neck, subclinical alterations of the vestibular function, intracranial hypertension, convulsion, hemiparesis, and generally includes motor components, among others. On the other hand, pure peripheral sensory disturbance has not been described. In this article, we report the clinical case of a patient with Charcot's arthropathy secondary to pure peripheral sensory polyneuropathy as a consequence of progressive herpetic encephalitis sequelae. In this article, the authors report the first case of Charcot's arthropathy secondary to herpetic encephalitis.

Wrist involvement in Hansen's disease.

We performed a neurological and radiological study of the wrists of 58 patients with Hansen's disease and 60 age-matched healthy control subjects. Significant differences (p < 0.01) were found between the groups in the carpal glenoid sector, the radial physeal widening index, the carpal ulnar distance, the carpal index and in distal radio-ulnar discrepancy. Comparison of the results in three subgroups of leprous patients with sensory impairment (group A-1), motor deficit (A-2) and no neurological impairment (A-3), showed significant differences (p < 0.01) between group A-1 and the other two. This suggests that in these patients the changes in the carpus and radiocarpal joint may be caused by neuropathic arthropathy of the wrist. Our findings are of particular interest since there are few reports of neuropathic arthropathy in non-weight-bearing joints.

The results of arthrodesis of the ankle for leprotic neuroarthropathy.

Twenty-four patients who had arthrodesis of one or both ankles for leprotic neuroarthropathy were followed for an average of nine years and five months. At operation, after the removal of cartilage, joint debris, and sclerotic bone, the ankle joint was transfixed with a Küntscher intramedullary nail, and staples or Kirschner wires were used to control rotation. Fusion of bone was obtained in nineteen (73 per cent) of the twenty-six ankles. Failure to obtain fusion was due to postoperative infection in four patients, deficiency of the site of arthrodesis in one patient, and refracture through the site of fusion in two patients. When arthrodesis was successful, additional neuroarthropathic destruction of the mid-tarsal joint was halted, and the preoperative clinical symptoms of dull pain, local warmth, swelling, and instability were relieved.

Arthropathy of the wrist in leprosy--what changes are caused by long-standing peripheral nerve palsy?

A radiographical screening study of 338 leprotic patients was performed. Clinically, according to a nerve score (NS) designed by us, 12.9% of 674 hands showed mild nerve palsy (NS 5 or 6), 75.9% moderate (NS 3 or 4), and 11.4% severe (NS less than 2). Twenty-nine hands of 26 patients (NS 4.2 on average) demonstrated abnormal changes of the wrist joint on radiographs. We classified them into four groups: (a) lunate collapse (four patients), (b) scaphoid nonunion (eight), (c) scaphoid cyst (three), and (d) trapezium OA (11). In the lunate collapse and the scaphoid nonunion groups, destructive and reconstructive changes as described by Eichenholtz were identified on plain film. These groups demonstrated remarkable instability of the stress and dynamic roentgenograms. In contrast, the scaphoid cyst and trapezium OA wrists showed neither fracture nor instability and fewer changes than the other two groups. We considered the destructive changes that had taken place in the lunate collapse and the scaphoid nonunion wrists to be neuroarthropathy due to long-standing nerve palsy.

Neuroarthropathy of the foot in leprosy.

Among 449 patients with leprosy, 40 had clinical and radiographic evidence of neuroarthropathy in 50 feet. These changes were classified into four types according to the joints first involved by major lesions: ankle (25 feet), midtarsal (15 feet), tarsometatarsal (7 feet) and subtalar (3 feet). The progression of joint destruction was different in each type, but despite the severe destructive changes seen in radiographs, the patients had relatively few complaints. The muscles innervated by the peroneal nerve were severely paralysed in ankle and midtarsal types and it seems that, over a long term, repeated trauma and/or abnormal stress may lead to these types of neuroarthropathy. Neuropathy was less severe in the tarsometatarsal type of joint degeneration; the pathogenesis in this type seemed to be mainly direct trauma to the forefoot.

Radiological changes in serial x-rays of the foot and tarsus in leprosy.

Most bone abnormalieis seen in serial films of the feet in leprosy were static being the end result of old disease. Changes over a period of time were observed in serial fims of 214 feet and these changes were due to a combination of infection, neuropathic changes and avascular necrosis occurring in anaesthetic feet. The bone abnormalities seen were absorption of toes and metatarsals; bone destruction; a neuropathic arthropathy of toes and metatarsals and various patterns of tarsal disintegration.