Phencyclidine: A Rare Cause of Saccadic Intrusions.

Saccadic intrusions such as opsoclonus and ocular flutter are often due to a paraneoplastic or a parainfectious condition. Toxins/drugs may rarely cause them. Herein, we report a rare case of ocular flutter/opsoclonus due to phencyclidine (PCP) toxicity. Our patient is a 21-year-old male who presented with a 3-day history of headache, generalized ill health, and aggressive behavior. He was admitted with reduced level of consciousness following generalized seizures. He had features of sympathetic overactivity with ocular flutter and opsoclonus. Urine toxicology was positive for PCP. Despite supportive care, he succumbed to complications of rhabdomyolysis. Several drugs including cocaine, phenytoin, lithium, and amitriptyline are known to cause ocular flutter/opsoclonus rarely. It is poorly described with PCP. This case highlights PCP as a rare cause of toxin-induced saccadic intrusions and attempts to postulate its pathogenesis. Moreover, our report is the first case of PCP intoxication in Sri Lanka and one of the few documented reports in the South Asian region. Therefore, it represents a significant worrisome alarm about the spread of this substance in this region.

Association of type IV spinal muscular atrophy (SMA) with myoclonic epilepsy within a single family.

BACKGROUND: Spinal muscular atrophies (SMAs) are a group of disorders characterized by degeneration of the anterior horn cells in the spinal cord and motor nuclei in the lower brainstem. It is transmitted by autosomal recessive inheritance and most of these conditions are linked to SMN gene. Even if the clinical picture is mainly dominated by the diffuse muscular atrophy, some patients can also show atypical clinical features such as myoclonic epilepsy ("SMA plus"), which may be related to other genes. In particular, the association of SMA and progressive myoclonic epilepsy (PME) has been previously described. CASE PRESENTATION: We present a case of two brothers with late onset SMA associated with a unique form of non progressive myoclonic epilepsy without cognitive impairment or ataxia. They had identical clinical and electrophysiological features. CONCLUSIONS: The association of SMA with myoclonic epilepsy may constitute a separate and genetically independent syndrome with unique clinical and electrophysiological findings. Collection of similar cases with genetic studies is needed to define the phenotype clearly and to identify new genes and molecular pathogenetic mechanisms involved in this condition.

Cryptococcal meningitis presenting with bilateral complete ophthalmoplegia: a case report.

BACKGROUND: Cryptococcus neoformans is saprophytic encapsulated yeast. Infection is acquired by inhalation of the organism and could be asymptomatic or limited to the lungs, specially in the immunocompetent host. Cryptococcal meningitis is a serious opportunistic infection among post transplant recipients. Cranial nerve palsies and ophthalmoplegia are well known complications of this disease, but bilateral complete ophthalmoplegia is a very rare presentation. CASE PRESENTATION: A Sri Lankan young male, who is a post kidney transplant recipient, presented with bilateral complete ophthalmoplegia and subsequently was diagnosed to have cryptococcal meningitis based on Indian ink stain and culture of cerebrospinal fluid (CSF). His magnetic resonance imaging (MRI) showed bilateral multiple nodular lesions in both basal ganglia and thalami. Brainstem imaging was normal. CONCLUSIONS: Cryptococcal meningitis is a serious fungal infection in post transplant patients. It should be suspected in any immunocompromised patient with fever, headache and focal neurological signs. Bilateral thalamic lesions, inflammation and invasion of the cranial nerves and raised intracranial pressure were thought to be possible mechanisms resulting in bilateral complete ophthalmoplegia in this patient.