1.Recurrent sixth nerve palsy in childhood ophthalmoplegic migraine: A case report
Chaudhry Neera ; Patidar Yogesh ; Puri Vinod ; Geeta A Khwaja
Neurology Asia 2013;18(1):95-98
Ophthalmoplegic migraine is a rare disorder characterized by childhood onset recurrent attacks of
migraineous headaches with paresis of ocular cranial nerves. The third cranial nerve is commonly
involved. Involvement of fourth and sixth cranial nerve is uncommon. We present a child with
opthalmoplegic migraine with recurrent sixth cranial nerve palsy on two occasions.
2.Intracranial hypotension due to shunt over drainagepresenting as reversible dorsal midbrain syndrome
Meena Gupta ; Yogesh Patidar ; Geeta A. Khwaja ; Debashish Chowdhury ; Amit Batra ; Abhijit Dasgupta
Neurology Asia 2014;19(1):107-110
Intracranial hypotension syndrome is an uncommon manifestation of shunt overdrainage; characterized
by a triad of postural headache, diffuse pachymeningeal gadolinium enhancement and low cerebrospinal
fluid opening pressure. We describe a young female with recurrent episodes of postural headaches
and reversible dorsal midbrain syndrome due to intracranial hypotension as a complication of shunt
overdrainage, and a subsequent improvement following shunt ligation.
3.Persistent cerebellar ataxia with cerebellar cognitive affective syndrome due to acute phenytoin intoxication: A case report
Meena Gupta ; Yogesh Patidar ; Geeta A. Khwaja ; Debashish Chowdhury ; Amit Batra ; Abhijit Dasgupta
Neurology Asia 2013;18(1):107-111
Phenytoin is one of the commonly used antiepileptic drugs. The common dose dependent and reversible
neurological side effects of phenytoin are nystagmus, diplopia, dysarthria, ataxia, incoordination,
chorioathetosis, orofacial dyskinesias and drowsiness. Persistent cerebellar dysfunction with cerebellar
atrophy is a well known complication of long term phenytoin use. There are several mechanisms
proposed including hypoxia due to frequent seizures or toxic effects of phenytoin on cerebellar Purkinje
cells. However, irreversible cerebellar dysfunction following acute phenytoin intoxication is rare. We
report a 20 year old female who presented with nystagmus, dysarthria, limb and truncal ataxia with
orofacial dyskinesias and chorea. She also had cognitive and affective symptoms in the form of reduced
attention, slow responses, lalling speech, blunting of affect, inappropriate laughter, reduced self care
and executive dysfunction. The symptoms started 2 weeks following the initiation of phenytoin 300mg/
day, given prophylactically following left basal ganglia bleed. Her serum phenytoin was in toxic range,
hence phenytoin was stopped. Her PET scan revealed bilateral cerebellar hypometabolism. At 6 months
follow up, she had persistent ataxia with cognitive and affective dysfunction and follow up MRI
showed diffuse cerebellar atrophy. The clinical and radiological fi ndings suggest that acute phenytoin
intoxication is responsible for persistent ataxia and cerebellar cognitive affective syndrome.
4.Progressive multifocal leukoencephalopathy in an immunocompetent patient: A case report
Meena Gupta ; Amit Batra ; Yogesh Patidar ; Debashish Chowdhury ; Geeta A. Khwaja ; Medha Tatke
Neurology Asia 2012;17(1):67-69
Progressive multifocal leukoencephalopathy (PML) is a progressive lethal demyelinating disease
of the brain, caused by JC virus. Reactivation of JC virus due to reduction of cellular immunity
especially in setting of AIDS, is the commonest underlying cause. PML has classically been described
in individuals with profound cellular immunosuppression such as patients with AIDS, haematological
malignancies, organ transplant recipients or those treated with immunosuppressive or immunomodulatory
medications for autoimmune diseases. Rarely it has also been diagnosed in cases with no or minimal
immunosuppression. Here, we report a 50 year-old man who presented with sudden onset multiple
neurologic defi cits. Neuroimaging, histopathology, and virology studies confi rmed the diagnosis of
PML. We could not however demonstrate any underlying immunodefi ciency state. Our case suggests
that absence of immunodefi ciency does not exclude the possibility of PML and should be considered
in immunocompetent patients with a typical clinical course and neuroimaging fi ndings.