Treatment of segmental continuous hypertrophic myokymia of the limb with botulinum A toxin.

Myokymia is defined as fluctuating hyperexcitability of muscle fibers caused by repetitive spontaneous contraction of motor units. Myokymia is generally benign with self-resolution, although symptomatic treatment with benzodiazepines, anticonvulsants, and muscle relaxants can be used. Botulinum toxins can also be utilized, although they are mostly used for symptomatic facial myokymia. Here, we report two patients who developed continuous myokymia, resulting in secondary hypertrophy, stiffness, and discomfort in the affected muscles. The first patient had a history of a tethered spinal cord and developed continuous myokymia in the S1 and S2 radicular regions of the left leg. The second patient underwent radiation therapy for lung cancer and developed brachial plexopathy with abnormal activity in the muscles supplied by the musculocutaneous nerve in the right arm. Both patients experienced sleep disturbance, focal discomfort, and restlessness. The anticonvulsants and muscle relaxants were ineffective. Chemodenervation with botulinum A toxin was initiated using either onabotulinumtoxinA or abobotulinumtoxinA. Both patients experienced a substantial reduction in myokymia, with ongoing reversal of muscle hypertrophy and significant improvement in reported subjective symptoms. Treatment with botulinum toxins can be highly effective in patients with symptomatic segmental continuous hypertrophic myokymia and may be considered first-line therapy.

Pseudotumor Cerebri Syndrome Without Headache in an Obese Male With Eight Restricted Cerebrospinal Fluid (CSF) Oligoclonal Bands: A Case Report.

Pseudotumor cerebri syndrome (PTCS) is a condition caused by an abnormal elevation of intracranial pressure (ICH), which may be primary (idiopathic intracranial hypertension) or because of an identifiable secondary cause. We present a rare case of an obese male who complained of gradual bilateral vision loss for one year without headaches and tinnitus. On fundoscopy, he had high-grade bilateral papilledema and, on lumbar puncture, he had an elevated intracranial pressure of 260 mmH2O. Cerebrospinal fluid (CSF) was unique for eight restricted oligoclonal bands while extensive other demyelinating workup was negative. He was started on acetazolamide initially and subsequently proceeded with bilateral optic nerve sheath fenestration (ONSF) with mild improvement in the right eye and no improvement in the left eye. Although the causative mechanism of PTCS is a matter of debate, immune-mediated processes are one of the proposed mechanisms that may play a role in the pathophysiology of PTCS, evidenced by the presence of oligoclonal bands (OCBs) and pro-inflammatory markers in CSF. PTCS diagnosed in men and patients with OCBs poses an increased risk of vision loss as this case and literature documented. Therefore, prompt treatment through therapeutic lumbar punctures, acetazolamide therapy concurrently with weight loss, and surgical intervention in severe or refractory cases are necessary.