Somatosensory evoked potentials following trigeminal nerve stimulation can regularly be recorded from the contralateral scalp on C5/C6 (10--20 system), a region which overlies the primary face region of the somatosensory cortex. From the first three peaks analyzed (N 13, P 19 and N 26), the first positive peak (P 19) is most prominent and reliable and therefore is recommended for the routine measurements of neurophysiological examination.
The examination of somatosensory evoked potentials following trigeminal nerve stimulation in 20 subjects with idiopathic trigeminal neuralgia revealed a pathological increase in latency of the first positive component on the involved side in 7 (41%) of the 17 patients without antecedent surgical treatment. The mean difference in latency between the two sides was 1.3 msec (2p greater than or equal to 0.005). These results are indicative of microtraumatization of the trigeminal nerve in the posterior fossa by blood vessels, for example, leading to local demyelinization. The method seems to be of diagnostic value in selecting patients for more decompression by posterior fossa operations.
In the CTS the motor nerve conduction velocity proximal to the wrist is reduced in proportion to the degree of severity of the nerve lesion. Furthermore the evoked nerve action potential is significantly reduced when recordings are made from the median nerve at the elbow and when the compound nerve is stimulated proximal to the lesion at the wrist. The extent of the retrograde changes correlates with the degree of severity and duration of nerve compression. Measurement of the evoked nerve action potential in the proximal nerve segment enables us to estimate the extent of the retrograde nerve fiber degeneration and therefore might be important for prognosis.
82 patients with chronic pain resulting from mononeuropathy were treated with psychotropic drugs in an open therapeutic study. In this study we found that treatment with a combination of clomipramine (Anafranil®) and small doses of neuroleptics was significantly superior to therapy with neuroleptics alone. In a subsequent double-blind study, it was attempted for the first time to determine the efficacy of clomipramine compared to that of acetylsalicylic acid in 48 patients with painful mono- and polyneuropathies. The test was carried out in a cross-over trial with two sequence groups. We evaluated assessments of pain by both patients and doctors, and were able to prove statistically that clomipramine possesses a significantly greater efficacy compared to that of acetylsalicylic acid. By taking into account recent anatomical, biochemical and pharmacological studies, it can be concluded that clomipramine probably has - in addition to the action on peripheral receptors - a direct effect upon pain modulation systems. It seems possible that clomipramine activates serotonin-containing neurons of the endorphin-mediated analgesia system that control pain transmission in the CNS.
The activities of the red blood cell enzymes transketolase, glutathione reductase, and glutamic oxaloacetate transaminase were measured with and without in vitro addition of their respective coenzyme components thiamine, riboflavin, and pyridoxine in a group of patients with neurological disorders which may have been caused by malnutrition, intestinal malabsorption, hepatic failure or neoplasms arising outside the nervous system. The incidence of thiamine deficiency was 31%, of riboflavin deficiency 22% and of pyridoxine deficiency 6%. Alcoholics in particular suffered from deficiencies of vitamin B 1, and B 2. There was a correlation of vitamin B 1 and B 2 deficiency and signs of a cerebellar and/or brainstem lesion. The most frequent symptoms in this connection were gait disturbances and oculomotor signs like spontaneous and gaze nystagmus, disturbed eye tracking, diminished optokinetic nystagmus, decreased ability to suppress vestibular nystagmus by fixation. These signs hardly ever occurred in alcoholic patients who showed no deficiency of vitamin B 1, B 2 or B 6. Whenever they do appear, a vitamin B supplementation has to be performed in order to prevent the manifestation of Wernicke's encephalopathy, cerebral or cerebellar atrophy. Alcoholics showed the same incidence of polyneuropathy, whether they suffered from a deficiency of B vitamins or not. Deficiencies of vitamin B 1, B 2 or B 6 were also found in patients with intestinal malabsorption and polyneuropathy, diabetic polyneuropathy, optic atrophy, myelopathy and cerebellar ataxia of unknown etiology, neurological manifestations of neoplasms arising outside the nervous system, B 12 myeloencephalopathy and Thévenard's syndrome.
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