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At least 937 records · Page 52Linked to original sources
PubMed1979

The afferent pupillary defect in acute optic neuritis.

Twenty-two patients with acute optic neuritis were studied by the techniques of infrared pupillometry and visual evoked responses (VER) to pattern reversal. A relative afferent pupillary defect was found in all cases and the magnitude of this defect was found to be related to the amplitude, but not to the latency, of the VER. During follow-up the afferent defect was found to remain persistently abnormal while other methods of clinical evaluation could not demonstrate abnormality reliably. The amplitude of the VER also remained low.

Acute Disease↗
PubMed2003

Vestibulo-ocular arreflexia in families with spinocerebellar ataxia type 3 (Machado-Joseph disease).

OBJECTIVE: To identify the presence of vestibulo-ocular arreflexia in patients with Machado-Joseph disease (MJD), which can easily be diagnosed at the bedside. METHODS: Seven patients with MJD from five unrelated families and 11 patients with sporadic or hereditary cerebellar ataxia other than MJD underwent a detailed neuro-otological and oculomotor examination. Six MJD and five non-MJD patients also underwent electro-oculographic recordings and caloric tests. RESULTS: Gaze evoked nystagmus, smooth pursuit, and saccade abnormalities were found in both MJD and non-MJD patients. However, in all seven MJD patients but in none of the non-MJD patients, sudden passively induced head thrust to both sides elicited pathological corrective catch-up saccades, indicating bilateral loss of the horizontal vestibulo-ocular reflex. This was further confirmed in six MJD patients who had absent vestibular response to both a standard caloric test and ice water ear irrigation. Nystagmus was induced by standard caloric irrigation in all non-MJD patients examined. There was no correlation between the loss of vestibular function and the severity of cerebellar impairment. CONCLUSIONS: The presence of vestibulo-ocular arreflexia, as measured by the head thrust test in a patient with dominant cerebellar ataxia, strongly suggests the diagnosis of MJD.

Adult↗
PubMed1991

[Relationship between electroencephalographic abnormality and late blink reflex responses in infantile spasms and EIEE].

Electrically elicited blink reflex (BR) were analyzed in seven patients with age dependent epileptic encephalopathies (5 patients with infantile spasms and 2 with EIEE). Four patients with infantile spasms showed prolonged latency of the late BR responses (R2). In 2 patients with EIEE showing suppression burst pattern on EEG, R2 was not detectable. R2 abnormality in BR might reflect the dysfunction of the brainstem reticular formation in age dependent epileptic encephalopathies.

Age Factors↗
PubMedDate not supplied

Positional nystagmus of central type and its neural mechanism.

Observations of Hallpike (1967) suggested that the neural mechanism responsible for positional nystagmus of central type, the direction-changing type of Nylén, was dependent upon derangement of compensatory eye reflexes subserved by neck proprioceptors and/or otolith organs in the presence of damage to the medial vestibular nuclei. Clinical studies together with autopsy evidence have demonstrated that this phenomenon may present in the absence of otolith function thus confirming Hallpike's thesis that positional nystagmus of central type may well depend on an abnormal neck reflex.

Brain Diseases↗
PubMed2003

Urinary dysfunction in patients with systemic lupus erythematosis.

AIMS: Nervous system involvement occurs in about half of patients with systemic lupus erythematosis (SLE). Seizures and psychiatric disorders are the most common manifestations; spinal cord lesions are uncommon. We had eight such patients who presented with urinary dysfunction. METHODS: The patients consisted of two men and six women, mean age 42 years, range 28-72 years. All patients were suffering from SLE for 2-25 years under immunosuppressant therapy. Their neurological manifestations were subacute encephalomyelopathy in three, subacute myelopathy in one, and chronic myelopathy in four. Urinary dysfunction included voiding difficulty in six (two of them had urinary retention initially) and urinary incontinence in four. Standard urodynamic studies were performed in the patients 2-3 weeks after admission. RESULTS: All patients had urodynamic abnormalities, including decreased urinary flow in five, increased post-void residual urine in three (mean 97 ml), increased maximum urethral closure pressure in two, detrusor hyperreflexia (DH) in five, impaired detrusor contractility in five, detrusor-sphincter dyssynergia in four, and neurogenic motor unit potentials of the external sphincter in two of four patients studied. DH was more common in patients with brisk deep tendon reflex (80%) than in those without (33%). Repeated studies showed that one had loss of bladder sensation, one developed a low compliance bladder, and one had decreased bladder capacity from 470 to 40 ml with marked DH during 2 months to 8 years follow-up period. CONCLUSIONS: Our results suggest that urinary dysfunction can be a feature in SLE patients is most commonly due to, and, in some patients there myelopathy, may be involvement of the spinal cord in a small group of the patients.

Adult↗
PubMed1999

Targeted inactivation of Hoxb8 affects survival of a spinal ganglion and causes aberrant limb reflexes.

Hoxb8 mutant mice were generated by inserting the lacZ coding sequence in frame with the first exon of Hoxb8. These mice express a fusion protein with a functional beta-galactosidase activity instead of Hoxb8. Mutant embryos were analyzed for anatomical changes. The results indicate that Hoxb8 is not an indispensable regulator of A-P patterning in the forelimb, unlike suggested by our Hoxb8 gain of function experiments (Charité J, DeGraaff W, Shen S, Deschamps J. Cell 1994;78:589-601). The null mutant phenotypic traits include degeneration of the second spinal ganglion (C2), an abnormality opposite to the alteration in the gain of function transgenic mice. Subtle changes in the thoracic part of the vertebral column were observed as well. Adult homozygous mutants exhibit an abnormal clasping reflex of the limbs.

Animals↗