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Pertinent information concerning the pupil is provided for the practicing and aspiring neurologist, including anatomy and physiology of the normal pupil, a discussion of pupillary disorders, and unusual pupillary abnormalities.
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Although the cause of myasthenia gravis is still unknown, its pathogenesis appears clear: immunologic attack on synaptic receptors in muscle causes receptor deficiency, decreased miniature endplate potentials, and decrements in the compound action potentials evoked from muscles on repetitive stimulation of peripheral nerves. In addition to the involvement of skeletal muscle, some MG patients may manifest subtle alterations of the function of heart, lung, smooth muscle, and CNS, indicating that this is truly a systemic disorder. Modern therapy involves adjusting treatment to the needs of individual patients. Anticholinesterases, calcium, ephedrine, potassium, and germine partially correct the defect in neuromuscular transmission; prednisone, ACTH, cytotoxic drugs, antilymphocyte serums, gamma globulin, thoracic duct drainage, plasmapheresis, and thymectomy partially modify the abnormalities of the immune system.
Eighteen patients with intracranial trigeminal nerve lesions were investigated electrodiagnostically. The trigeminal motor root function was studied on the basis of the jaw reflex and masseter myograms and was disturbed in all cases. The jaw reflexes were abnormal in 16 and the masseter myograms in eight cases. An impressive trigeminal sensory root function was obtained from blink reflex, which was abnormal in 12 cases. The results show the diagnostic value of bilateral recording of the jaw reflex in such patients.
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Cardiovascular effects of diabetic autonomic neuropathy include postural hypotension, resting tachycardia, and, possibly, painless myocardial infarction. Involvement of cardiovascular reflexes in diabetes can be assessed using simple noninvasive tests: the Valsalva maneuver, beat-to-beat heart rate variation, the heart rate response to standing, postural fall in blood pressure, and the sustained handgrip test. Tests of parasympathetic function appear to be abnormal more frequently and earlier in cardiac autonomic involvement, whereas sympathetic damage usually occurs later and is associated with clinical symptoms. When test results are abnormal, in association with symptoms suggestive of autonomic neuropathy, the prognosis is grave. Some sudden deaths that occur may be due to abnormal autonomic reflexes.
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OBJECTIVE: To study the startle reflex and the effect of the startle reflex stimulus over reaction time (start-react effect) in Gilles de la Tourette syndrome (GTS). METHOD: Ten GTS patients and ten matched healthy volunteers underwent a simple RT paradigm (4 blocks of 50 trials). Forty acoustic startle reflex stimuli (110 dB) were randomly delivered with a 20% occurrence probability and presented unexpectedly at the same time as the imperative stimuli of the RT. Variables of interest were: amplitude, onset latency, degree of spread and rate of habituation of the startle response, and RT and the start-react effect caused by the startle stimuli. RESULTS: GTS patients showed a significantly higher amplitude, a major degree of spread and fewer habituation phenomena of the startle reflex. GTS patients showed poorer non statistically significant RT performance compared to controls, with a significant correlation between RT and severity of the disease. The start-react effect was significantly less pronounced in GTS patients. CONCLUSIONS: The present study confirms that GTS has an exaggerated startle reflex response and extend the spectrum of abnormalities to the start-react effect. A state of dopaminergic hyperactivity may have contributed to these results.
A method is described to obtain suitable parameter values for an adaptation model that can be used to simulate velocity step (VS) responses. The input parameters are the dominant time constant fitted to the first part of the VS response and the time of reversal in nystagmus direction. This method allows a particular solution for the model previously defined by others with a vestibulo-ocular reflex (VOR) time constant, a time constant of adaptation, and a fixed (unitary) gain of the adaptation element. However, because it might be arbitrary to assume a unitary gain, we also studied a more general model with a variable gain element. It appeared that patients showing short responses had a short VOR time constant and less adaptation than normal. Patients exhibiting prolonged responses appeared to have an excessively long VOR time constant and more adaptation than normal, presumably to compensate for the long time constant.
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