Juergen E. Thomas

Differential diagnosis between radiation and tumor plexopathy of the pelvis

We studied 20 patients with lumbosacral radiculoplexopathy from radiation treatment and 30 patients with plexus damage from pelvic malignancy. Indolent leg weakness occurred early in radiation disease, whereas pain marked the onset of tumor plexopathy. Eventually, all radiation cases had weakness, which was bilateral in most of them and painless in one-half of them. Tumor patients typically had unilateral weakness, which was painful in all of them. Radiation disease often resulted in serious neurologic disability. Of the tumor patients, 86% were dead within 31/2 years after onset of neurologic symptoms.

Thermoregulatory Sweating Abnormalities in Diabetes Mellitus

A properly performed thermoregulatory sweat test (TST) can be informative in patients with diabetic neuropathy. Of 51 patients suspected of having neuropathy on the basis of a clinical examination, 48 (94%) had unequivocal abnormalities on the TST. Pathologic loss of sweating occurred distally in 65%, segmentally in 25%, and only in isolated dermatomes in 25%; 78% of patients had a combination of two or more patterns. Global anhidrosis was noted in eight patients (16%), all of whom had profound autonomic neuropathy, and in the entire group, the percentage of body surface anhidrosis correlated with the degree of clinical dysautonomia (rank correlation coefficient = 0.77; P less than 0.01). Discrete zones of anhidrosis on the thorax and abdomen were noted in patients with painful diabetic radiculopathy, and they correlated highly with thoracic paraspinal muscle fibrillation potentials. Distal loss of sweating detected on the TST was always associated with a subnormal quantitative sudomotor axon reflex response or abnormal electromyographic findings, an indication of a distal axonal neuropathy. The TST provides reliable information about the distribution of diabetic neuropathic involvement and can be especially useful in the diagnosis of truncal radiculopathy and clinically significant autonomic neuropathy.

Segmental zoster paresis—a disease profile

In the presence of appropriate cutaneous manifestations, it is seldom arduous to decide whether segmentally distributed pain is the result of herpes zoster. Less well known is the fact that motor neurons have no immunity to the infection and that muscle weakness of profound degree may be part of the zoster syndrome. The diagnosis, at first so reassuringly simple, may suddenly seem in doubt when paresis occurs weeks after the skin rash has subsided or weakness transgresses the boundaries of the cutaneous segment. muscle weakness, a total of 66. Five of these were not appropriate to our study and were excluded (encephalitis, 2; myelitis, 1; and neuronitis, 2). Retained for final analysis were 6 1 cases with segmental zoster paresis.

Distinction between neo plastic and radiation‐induced brachial plexopathy, with emphasis on the role of EMG

results of clinical, radiologic, and electro physiologic studies are retrospectively reviewed for 55 patients with neo plastic and 35 patients with radiation-induced brachial plexopathy. The presence or absence of pain as the presenting symptom, temporal profile of the illness, presence of a discrete mass on CT of the plexus, and presence of myokymic discharges on EMG contributed significantly to the prediction of the underlying caw of the brachial plexopathy. The distribution of weakness and the results of nerve conduction studies were of no help in distinguishing neo plastic from radiation-induced brachial plexopathy.

Assessment of roentgenographic lucencies of the skull A systematic approach

A review of roentgenologic characteristics of cranial vault defects suggests these criteria as favoring benign etiology: solitariness and small size, parasagittal location, smooth edges, sclerosis of margin, peripheral vascularity, and presence of bone remnants within the lesion. The more of these criteria that are present, the greater is the likelihood of benignity. Conversely, the presence of multiple defects of large size or scores of defects of small size, ragged undermined edges, total bone penetration, lack of peripheral vascularity, or absence of marginal sclerosis is presumptive evidence of malignancy.

Nonhemorrhagic complications of intracranial aneurysms of the internal carotid artery

SUMMARYNonhemorrhagic complications of intracranial aneurysms of the carotid artery often follow a recognizable neurological pattern. The brunt of the deficit is borne by the anterior cranial nerves, either singly or in combination. Depending on the location of the aneurysm, further trends of selective involvement are evident. Infraclinoid extradural carotid aneurysms classically attack the cranial nerves III, IV, V, and VI but often spare the optic nerve. By contrast, supraclinoid intradural carotid aneurysms typically affect the optic nerve or chiasma or both, leaving the extraocular muscle nerves relatively unaffected and sparing the second and third divisions of the trigeminal nerve. Severe frontal or orbital pain from involvement of the first trigeminal division is the most frequent and, commonly, the earliest symptom, regardless of aneurysmal location. Evolution of symptoms and signs varies. Progressive stepwise deterioration or a course punctuated by exacerbations and remissions prevails. Neurological deficit, although characteristic of aneurysm, is not pathognomonic. Other intracranial lesions with similar manifestations must be considered.

Evaluation of the Comatose Patient

The authors discuss the value of a prepared methodical plan of action in evaluating the comatose patient. They stress the importance of first recognizing and correcting any respiratory or circulatory failure, and then thoroughly assessing the history and results of physical examination. Laboratory tests which are likely to yield maximal information in the shortest possible time while causing the least discomfort to the patient should be selected. The finding of an obvious abnormality early in the evaluation does not justify an incomplete appraisal since other diseases may be coexistent, particularly if the coma has been present for considerable time. Timely discovery of the cause of coma often will permit institution of lifesaving therapy.