Biomedical subjects
Publications and source records attributed to M Mumenthaler.
This survey describes the main neurological alterations which are observed in the diabetic foot. They consist of 1) painful sensations 2) distal disturbances of sensitivity 3) absent reflexes of the Achilles tendon 4) trophic ulcers 5) impaired arterial circulation 6) deformities of toes and foot. The characteristics of these various alterations are enumerated.
The principles of neurological examination of patients in which psychogenic disturbances are suspected are first described. After mentioning the frequency of this type of disturbances in the medical literature, some of the most characteristic and most frequent psychogenic disturbances in neurology are described: cranial nerve symptoms, sensory disturbances as well as psychogenic paralysis including paraplegia and psychogenic disturbances of gait. A chapter is dedicated to psychogenic disturbances of consciousness and to psychogenic attacks mimicking epilepsy. Finally a description is given of those organic neurological diseases in which in our experience the erroneous diagnosis of psychogenic disturbances is most frequently made. Some recommendations, how to behave in the presence of a patient with psychogenic neurological symptoms is added.
To look for a correlation between positive antibody-response against Borrelia burgdorferi (Bb) and an inflammatory CSF-syndrome, from May 1988 to May 1989 333 patients from the Neurological Department of the University of Bern underwent lumbar puncture with cell count, quantitative and qualitative protein analysis and antibody determination against Bb in serum and CSF. 6 patients with active syphilis were excluded. The results of the 333 remaining patients were analyzed using chi 2 or Fisher's exact test. The antibody determination was performed using an immunoperoxidase assay (IPA). Our results are calculated for three cut-off points: Bb-IgG 1:64, 1:128, 1:256 and/or Bb-IgM 1:16, 1:32, 1:64. We found 11.7% patients to be seropositive (Bb-IgG 1: greater than or equal to 256 and/or Bb-IgM 1: greater than or equal to 64). We demonstrated the following correlations: elevated cell count (greater than 10/mm3 cells CSF) versus elevated Bb-titer (1: greater than or equal to 256), elevated total protein of CSF (greater than 48 mg%) versus elevated Bb-titer, blood-brain-barrier dysfunction versus elevated Bb-titer. In diagnostic subgroups, the same correlations were only demonstrated for PNS disorders (n = 134), and especially PNS-disorders without compression. 8 cases showed the high risk constellation inflammatory CSF syndrome and highly positive titer (Bb-IgG 1: greater than or equal to 256). Only 2 had typical neuroborreliosis, while in 2 cases the possibility of neuroborreliosis was open. Patients with MS did not show a special risk for Bb-infection.(ABSTRACT TRUNCATED AT 250 WORDS)
The value of brain CT-scan, magnetic resonance imaging (MRI) and angiography for diagnosis, differential diagnosis and follow up in Neuro-Behçet-Syndrome is assessed in 5 cases. Three of the patients presented with clinical signs of encephalitis. Further investigations led to the diagnosis of Behçet-Syndrome. CT-scan was negative in two of these cases, but MRI showed multiple, predominantly periventricular lesions with high signal intensity on T2-weighted spin-echo images in all three. Clinical symptoms improved with steroid and chlorambucil therapy in all three cases. In two patients the MRI-lesions resolved at least partially after 1.5 and 3 years of treatment respectively. In one patient the initial MRI-findings were still present after 7 months of treatment. The other two patients presented with headache, papilledema and increased CSF-pressure. The cause was superior sagittal sinus thrombosis, confirmed by angiography in both cases. Additional symptoms appeared later and led to the diagnosis of Behçet syndrome. One patient died of pulmonary aneurysms 28 months after the diagnosis had been established. The course of disease of the remaining patient is so far favorable.
Two patients with isolated neurogenic hypertrophy of the trapezius muscle due to accessory nerve injury and a patient with neurogenic hypertrophy of the anterior tibial muscle due to chronic radicular lesion L4 are described. Electromyography of the affected muscles showed dense continuing spontaneous discharges of complex potentials. Muscle biopsy performed in two patients showed abundant hypertrophic muscle fibres, identified in one case by ATP-ase reaction as being of predominantly type I. In the majority of previously reported patients with neurogenic muscle hypertrophy confined to the calf muscle, a passive stretch mechanism was suggested as a cause of the hypertrophy. It is assumed that the excessive spontaneous muscle activity gave rise to the hypertrophy in these patients. This may also be true in previously reported patients with neurogenic hypertrophy and similar spontaneous activity in electromyography.
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One out of three patients seeking the doctors advice complain about fatigue. Two out of three are fatigued because of psychological reasons. A systematic way of analysis of this symptom is described, as well as the characteristics of somatic fatigue syndromes as opposed to psychogenic ones. Finally a brief description is given of the main diseases accompanied by fatigue.
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Clinical, neurophysiological, morphological and biochemical investigations were performed in 2 patients with the adult form of glycogenosis II and related to the findings of 58 well-documented cases published in the literature. According to these findings three types can be distinguished from each other. The first one is characterized by an involvement of the limb-girdle muscles only. The second type shows the same pattern with additional progressive insufficiency of the respiratory muscles. The third type presents with weakness of the respiratory muscles without any other severe muscle involvement. Our case 1 can be related to the first, our case 2 to the second type. EMG-studies in case 1 showed myopathic changes and myotonic discharges without clinical signs of myotonia. A myotonic pattern was described in one third of the published cases. In case 2 neurogenic changes as well as in 4 cases in the literature were found. The muscle biopsy is the diagnostic clue in the differential diagnosis of progressive myopathy in the adult. Patients with glycogenosis II show glycogen storage specially in type I-fibres. The enzyme defect can be confirmed biochemically in muscle tissue or cultured fibroblasts. Various therapeutic concepts have been tried in patients with glycogenosis II but most of them remain disappointing. A diet with a low carbohydrate and a high protein proportion was observed to be of some benefit. In patients with respiratory muscle involvement artificial ventilation support showed a positive effect on the general condition for some time.
Some of the neuromuscular diseases may lead to respiratory failure. This is the case in some lesions of the anterior horn cells (poliomyelitis and spinal muscular atrophy), in diseases affecting the nerve roots (acute polyradiculitis and lesions of the C4-roots) or affecting the phrenic nerve. Respiratory failure is frequent in myasthenia and may accompany Duchenne's muscular dystrophy. In each case one has to evaluate the opportunity of respiratory treatment considering all the elements of the disease and of the individual patient.
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Loss of neurologic function with acute onset is a hallmark of cerebrovascular disease, but may have several other etiologies. Knowledge of the functional significance of the different brain areas and of their vascular supply is a prerequisite for localizing a lesion. Clinical presentation alone often does not allow etiological diagnosis, which eventually decides upon treatment modality. For that purpose, we need the help of various investigational techniques with different content of information. Their selection depends on individual anamnestic and clinical findings and has to consider the therapeutical possibilities in the individual case, too.
Elimination of vascular risk factors is of paramount importance in preventing stroke. Once a vascular pathology is present, various surgical and medical measures must be considered in order to lower the risk of cerebrovascular accident. When infarction has occurred, the therapeutic possibilities are limited and aim at reducing the size of a stroke. The authors review current issues in stroke prevention and treatment.
The anatomy, type, etiology, and functional classification of stroke are reviewed. Diagnostic techniques are outlined and a diagnostic plan is suggested which the authors consider reasonable.
We report on 3 patients with meningoradiculoneuritis (MRN) due to Lyme-borreliosis (LB), which presented clinically as vertebral disc herniation. In 2 cases the underlying infection was discovered only after unsuccessful neurosurgical treatment. In the differential diagnosis between MRN and disc herniation the following criteria are suggestive of MRN and should raise suspicion of a non-discogenic aetiology: History of tick bite or erythema chronicum migrans, fever or general malaise, mono- or oligoradiculopathy with absent or insignificant lumbar pain and complaints of a burning character of the radiating pain. In suspicious cases we recommend blood investigations including antibody determination against borrelia burgdorferi and CSF investigations including cell count and cytology, protein and glucose determination, nephelometry and isoelectric focusing to exclude MRN and other conditions that may mimic disc herniation.
Neurological signs and computed tomographic morphology were compared in 60 patients. The primary neurological deficit was most commonly located in the sacral (n = 31) or lumbar plexus (n = 23) and was most commonly caused by a neoplasm (n = 40). In 78% of the patients it correlated with the lesions detected by computed tomography (CT). CT reliably demonstrates extraspinal mass lesions, but only moderately well predicts functional signs.
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