Hereditary spastic paraparesis (HSP) can be an inherited group of neurological

Hereditary spastic paraparesis (HSP) can be an inherited group of neurological disorders with progressive lower limb spasticity. The patient’s father and younger sister suffer from pure HSP. The patient was diagnosed to have first episode mania with complicated HSP. The details of treatment and possible neurobiology are discussed in this case report. Keywords: Complicated hereditary spastic paraparesis hereditary spastic paraparesis mania Introduction Hereditary spastic paraparesis (HSP) or Strümpell-Lorrain syndrome is an inherited group of neurological disorders with progressive lower limb spasticity. HSP is classified into pure/uncomplicated and complicated/complex forms. HSP is transmitted through an autosomal-dominant (AD) autosomal-recessive (AR) or X-linked (XL) manner. An AD transmission accounts for 70-80% of all HSP.[1] It affects all the age groups and the prevalence of HSP ranges from 2.0 to 9.6/100 0 depending on different diagnostic criteria used and populations studied.[2] The cardinal abnormalities of patients with HSP include spasticity hyperreflexia urinary bladder disturbance (hypertonic bladder) and extensor plantar responses with weakness of a pyramidal distribution in the lower limbs. We report a case of a 17-year-old boy who presented with HSP and mania. The possible association of HSP with bipolar disorder has not been frequently resolved in the medical literature. Case Report A 17-year-old young man VX-809 reported to the Department of Psychiatry with complaints of excessive happiness irritability increased self-esteem and decreased BMP2 sleep since 1 month. The patient was known case of HSP with epilepsy since 7 years. He was born of a nonconsanguinous marriage. Details of family are pointed out in the family genogram [Physique 1]. The patient had episodes of staring twitching around the mouth grimacing followed by loss of consciousness and fall followed by involuntary jerky movements of the extremities. His seizures and neurological illness had both started simultaneously. The patient was taking Tab carbamazepine 400 mg/day for the last 5 years. Seizure episodes decreased after starting carbamazepine from three to four episodes in a 12 months to total absence of episodes in last 3 years. The patient’s father and sister also have HSP without any diagnosable psychiatric or epileptic disorders. All the affected family members had onset of HSP around 12 years VX-809 of age which had progressed for 3-4 years and later the condition became static. The patient’s mother had a history of paranoid schizophrenia; she had committed suicide 8 years VX-809 ago. Physique 1 Family genogram On general physical examination the patient was moderately built and nourished with normal vital parameters. He was conscious and well-oriented during examination. His neurological examination revealed that both his limbs were equally affected. There was increased muscle tone in the hamstring group and in the ankle region positive patellar clonus and Babinski’s sign brisk deep tendon reflexes wasting of distal muscle groups and spastic gait. There were no cranial nerve deficits cerebellar indicators and indicators of meningeal irritation. On mental status examination he was well kempt had increased psychomotor activity pressure of talk irritability elevated self-esteem and delusion of grandiosity. When baseline Young’s Mania Rating Size (YMRS) was used the rating was 26 and his baseline hematological and biochemical investigations had been within regular limitations. Computed tomography imaging didn’t reveal any abnormalities. Medical diagnosis of the initial bout of mania with psychotic symptoms was produced using ICD-10 DCR requirements.[3] The individual was independently interviewed by two competent psychiatrists to eliminate every other psychiatric disorders but testing instruments like SCID or MINI weren’t used. The individual was presented with Tab Sodium Valproate 500 mg Tab and bid/time Olanzapine 15 mg/time. Valproate was cross-tapered with carbamazepine over an interval of 14 days. Taking into consideration the poor response through the first 14 days with Olanzapine and an identical observation with the family the treating.