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Hemifacial spasm: location of the lesion by electrophysiological means.

In hemifacial spasm a late abnormal motor response was elicited by the antidromic volley after stimulating a peripheral branch of the facial nerve. The site of the lesion was calculated from the latency of that motor response and the conduction velocity. In 5 patients the distance was long, and corresponded with a tumor or a vascular anomaly at the cerebellopontine region in 3 of them. An artery sling entering the internal acoustic meatus was found in 2 out of 3 patients with short distances. It is concluded that hemifacial spasm results from a nerve lesion that may be located as far peripherally as the internal acoustic meatus. The theory of facial nuclear irritation is incompatible with such a peripheral lesion.

Cerebellopontine Angle↗

Hemifacial spasm: electrophysiological findings and the therapeutic effect of facial nerve block.

Twenty patients with cryptogenic hemifacial spasm have been examined electrophysiologically and treated with blockade of the facial nerve with phenol injections after localization of the nerve by electrical stimulation. The electrophysiological findings suggested a central origin of the spasms. The phenol injections abolished the spasms, but they recurred in most patients after 6 to 12 months. A few patients appeared to get permanent relief after one or more phenol injections. We used phenol blockade of the facial nerve as our first therapeutic treatment of choice in patients with distressing hemifacial spasm because it is a safe, simple, and repeatable procedure.

Adult↗

Hemifacial spasm: treatment by microvascular decompression of the facial nerve at the pons.

Hemifacial spasm is a syndrome of intermittent and tonic unilateral facial muscular contraction; mild facial weakness on the same side is also frequently present. Hemifacial spasm can be differentiated clinically from habit spasms, blepharospasm, facial synkinesis following Bell's palsy, facial myokymia, and masticatory spasm. The syndrome of hemifacial spasm is caused by a variety of lesions; the common feature appears to be compression of the facial nerve at the pons. Diagnostic studies do not usually add significant information to that gained from the history and physical examination. The best current treatment (aside from removing an etiologic lesion such as a posterior fossa tumor in the small percentage of cases with such lesions) is microvascular decompression of the facial nerve at the pons through a retromastoid craniectomy. Of 30 patients treated in this manner, 28 have been satisfied with the results. On the most recent follow-up examination, 16 had no hemifacial spasm, nine had only slight periodic twitching about the eye, and three had occasional mild episodes of hemifacial spasm.

Adult↗

[A 49-year-old man with progressive dysarthria, dysphagia, and left hemiparesis].

We report a 49-year-old man who presented progressive dysarthria, dysphagia, and left hemiparesis. The patient was well until June 28th of 1993 when he noted 'weakness' in his both legs; despite his weakness, he could play golf on that day. In the beginning of July, he noted difficulty in swallowing solid foods. He was admitted to the neurosurgery service of our hospital on July 15th of 1993 and a neurologic consultation was asked on July 17th. Neurologic examination at that time revealed an alert but somewhat childish man who appeared to have some difficulty in paying attention to questions. He was disoriented to time and showed difficulty in recent memory and calculation. Higher cerebral functions were intact. The optic fundi were normal; pupils were isocoric and reacted to light promptly; ocular movements were intact, however, he showed difficulty in convergence. Facial sensation and facial muscles were intact. He had no deafness. He showed slurred speech and difficulty in swallowing solid foods. The remaining cranial nerves were intact. Motor-wise, he was able to walk normally and no weakness or atrophy was noted. Mild ataxia was noted in the finger-to-nose and the heel-to-knee test on the left. Muscle stretch reflexes were normal and symmetric, however, the plantar response was extensor bilaterally. Sensation was intact and no meningeal signs were noted. General routine laboratory findings were unremarkable. CSF was under a normal pressure containing 1 cell/microliter, 68 mg/dl of protein, and 54 mg/dl of glucose. Cranial CT scan showed low density areas involving the pons, midbrain, left thalamus, and the left parietal cortex. In MRI, these areas presented low signal intensity in T1-weighted images and high signal intensity in T2-weighted in images. The brain stem appeared swollen. Gadolinium enhancement was negative. He was given a course of steroid pulse with 1 g/day of DIV methylprednisolone for three days followed by oral steroid. He showed only temporary improvement in swallowing. In the subsequent course, he showed progressive deterioration in dysarthria and dysphagia. A biopsy was performed on the left parietal lobe lesion. After biopsy, he was treated with steroid and glycerol without improvement. A course of chemotherapy with procarbazine, MCNU, and vincristine was given; he did not respond to chemotherapy. His left hemiparesis deteriorated. He developed aspiration pneumonia from dysphagia and expired on October 22, 1993. The patient was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had astrocytoma grade III involving the pons, midbrain, thalamus, and the parietal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain Neoplasms↗

[Subacute hypoglycemic encephalopathy: a case report].

A 63-year-old woman with long lasting diabetes, irregularly nourished and treated with oral antidiabetic drugs, developed hyperkinetic movements in the upper and lower extremities and facial muscles, as well as some disturbances of consciousness. The EEG showed generalized slowing of bioelectrical activity, serum glucose level was 69 mg%. Nevertheless after the antidiabetic drugs were withdrawn and the meals regulated, a normalization of the clinical picture and the EEG was observed. Therefore it seems that the patient was very sensitive to even minor hypoglycemia and the diagnosis of subacute hypoglycemic encephalopathy was made.

Blood Glucose↗

Temporomandibular dysfunction, chronic orofacial pain and oral motor disorders in the 21st century.

This article describes the various sensory and motor disorders that afflict the orofacial region. These abnormalities are broadly separated into three groups of pathologic conditions: temporomandibular disorders; chronic orofacial pain disorders; and oral motor disorders. This article focuses on the diagnostic features of each specific disorder, suggesting alternate nomenclature for each disorder.

Bruxism↗

[Study on pathogenic mechanism of hemifacial spasm].

In 17 cats, areas of focal injury were induced in the facial nerve root near the brain stem by implantation of V-clamp and catgut suture. The electrophysiological examinations were made at 3 weeks after the surgery. When the mandibular branch of the facial nerve was electrically stimulated, a combined activity potential and a delayed activity could be recorded from the orbicular ocular branch of the facial nerve. The delayed activity disappeared after the motornucleu of the facial nerve was blocked with injection of 2% Lidocaine(1.5 microliter). These phenomena suggests that the artifacial synapses have been formed among the demyelinating facial nerve. The antidromic impulse of the mandibular branch of the facial nerve spread to adjacent fibers through the artifacial synapses in REZ of the facial nerve and causes the synkinases and spasm. Delayed activity may be caused by neurons of the motornucleu. Experimental lesion was also examined histologically at 3 weeks following implantation. Injured nerve showed areas of demyelination and Waller's degeneration of adjacent axons. The Nissle substances at the neurons of the motornucleu were dissolved and disappeared.

Action Potentials↗