Tehran University Medical Journal

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Between 1371 to 1379, of 10 patients with radial tunnel syndrome, 9 patients were treated by decompression of the posterior interosseous nerve. 8 patients were followed up more than 10 months. One patient improved without surgery. Half of the patients suffered from pain and all of them had variable degrees of paralysis in muscles innervated by deep branch of the radial nerve. The syndrome was diagnosed after an average of 26 months after onset of symptoms. 3 patients had associated endocrine disease and 2 patients suffered from another accompanied compression neuropathy. 8 patients performed strenuous, repetitive upper extremity tasks. EMG confirmed the diagnosis in all patients. The source of nerve entrapment was identified as the arcade of Frohse in 4 patients. Malignant soft tissue tumor was responsible for nerve compression in one patient. More than one pathologic site was responsible for nerve entrapment in another 4 patients. Of 8 patients with enough follow-up after operation, pain was improved in all, but paralysis was improved in only half of them. According to ritts criteria, results were good in 50% of patients and in 50% of patients results were bad. All bad results were due to persistence of paralysis in affected muscles. One of four patients who had no improvement in paralysis, was satisfied with surgical result because tendon transfer was performed at the time of nerve decompression. It is recommended that all possible sites of nerve compression in the radial tunnel be explored and released.

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Autonomic nervous system dysfunction in diabetics can occur apart from peripheral sensorimotor polyneuropathy and sometimes leads to complaints which may be diagnosed by electrodiagnostic methods. Moreover glycemic control of these patients may prevent such a complications.
Materials and Methods: 30 diabetic patients were compared to the same number of age and sex-matched controls regarding to electrophysiologic findings of autonomic nervous system. Symptoms referable to autonomic disorder including nightly diarrhea, dizziness, urinary incontinence, constipation, nausea, and mouth dryness were recorded in all diabetic patients. Palmar and plantar SSR and expiration to inspiration ratio (E: I) and Valsalva ratio were recorded in all diabetics and control individuals by electromyography device. In addition NCS was performed on two sensory and two motor nerves in diabetic patients.
Results: There was no relation between age of diabetics and abnormal D: I ratio, Valsalva ratio and degree of electrophysiologic autonomic impairment. Also no relation between peripheral sensorimotor polyneuropathy and electrophysiologic autonomic impairment was found. Plantar SSR was absent in 80% of diabetics with orthostatic hypotension (p~ 0.019). Palmar and plantar SSR were absent in many diabetics in comparison to control group (for palmar SSR p~ 0.00 and for plantar SSR p< 0.015). There was no relation between diabetes duration since diagnosis and electrophysiologic autonomic impairment.
Conclusion: According to the above mentioned findings diabetic autonomic neuropathy develops apart from peripheral sensorimotor polyneuropathy and probably with different mechanisms. Remarkable absence of palmar SSR in diabetics with orthostatic hypotension can be due to its sympathetic origin. Absence of any relation between diabetes duration and electrophysiologic autonomic impairment can be due to late diagnosis of type 2 diabetes or no pathophysiologic relation between chronic hyperglycemia and autonomic neuropathy.

 

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Background: Diabetic neuropathy is an incapacitating disease that afflicts almost 50 percent of patients with diabetes. A late finding in type 1 diabetes, diabetic neuropathy can be an early finding in non insulin-dependent diabetes. Diabetic neuropathies are divided primarily into two groups, sensorimotor and autonomic. Patients may acquire only one type of diabetic neuropathy or may present with combinations of neuropathies, such as autonomic neuropathy or distal symmetric polyneuropathy, the latter of which the most common form. Motor deficits, orthostatic hypotension, silent cardiac ischemia, hyperhidrosis, vasomotor instability, gastroparesis, bladder dysfunction, and sexual dysfunction can also result from diabetic neuropathy. Strict control of blood sugar, combined with proper daily foot care, is essential to avoid the complications of this disorder. With the potential to afflict any part of the nervous system, diabetic neuropathy should be suspected in all patients with type 2 diabetes as well as patients who have had type 1 diabetes for over five years. Although some patients with diabetic neuropathy notice few symptoms, upon physical examination mild to moderately severe sensory loss may be noted by the physician. Idiopathic neuropathy has been known to precede the onset of type 2 diabetes.

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Background: Although it is not a new disorder, in recent times we have attained a greater understanding of auditory neuropathy (AN). In this type of hearing impairment, cochlear hair cells function but AN victims suffer from disordered neural transmission in the auditory pathway. The auditory neuropathy result profile often occurs as a part of that of the generalized neuropathic disorders, indicated in approximately 30-40% of all reported auditory neuropathy/auditory dyssynchrony (AN/AD) cases, with approximately 80% of patients reporting symptom onset over the age of 15 years. In the present report, the results of audiologic tests (behavioral, physiologic and evoked potentials) on two young patients with generalized neuropathy are discussed.
Case report: Two brothers, 26 and 17 years old, presented with speech perception weakness and movement difficulties that started at 12 years of age and progressed as time passed. In their last examination, there was a moderate to severe flat audiogram in the older patient and mild low tone loss in the younger one. The major difficulty of the patients was severe speech perception impairment that was not compatible with their hearing thresholds. Paresthesia, sural muscle contraction and pain, and balance disorder were the first symptoms of the older brother. Now he can only move with crutches and his finger muscle tonicity has decreased remarkably, with marked fatigue after a short period of walking. Increasing movement difficulties were noted in his last visit. Visual neuropathy had been reported in repeated visual system examinations for the older brother, with similar, albeit less severe, symptoms in the younger brother.
In the present study of these patients, behavioral investigations included pure-tone audiometry and speech discrimination scoring. Physiologic studies consisted Transient Evoked Otoacoustic Emission (TEOAE) and acoustic reflexes. Electrophysiologic auditory tests were also performed to determine Auditory Brainstem Response (ABR), Auditory Middle Latency Response (AMLR) and Auditory Late Response (ALR). The results of these examinations for these two siblings are discussed and compared with the results of other studies.
Conclusion: Distinguishing auditory neuropathy from other speech perception disorders can be performed by conducting audiologic evaluations as a battery of tests. The probability of generalized neuropathy must be considered in patients with auditory neuropathy symptoms.

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Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 Background: Lead poisoning could be associated with gastrointestinal renal, hematologic complications and neurologic deficit.
Case report: The patient was an opium addict, forty one years old male, to hospital admitted with gastrointestinal signs, constipation, abdominal pain, severe weakness of upper and lower limbs without any sensory impairment and with anemia, leukocytosis, and slightly increased liver function tests. Serum level of lead was more than 200µg/dl. After treatment with dimercaprol (BAL), CaNa2EDTA for two five days sessions that followed with oral succimer for three days, signs and symptoms relieved, all laboratory tests became normal and blood level of lead reduced but the patient was discharged with quadriplegia. There was no fecal or urinary incontinence.
Conclusions: Because of irreversibility and severity of lead related neuronal injury, we should suspect to lead poisoning in each patient with neuronal involvement and concurrent GI and hematologic signs.

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