Present and future of neurology in pakistan

Neurology started as a department in early nineteen sixties in Dow Medical College and King Edward Medical College and initially having a separate department of neurology was not mandated in medical colleges by Pakistan Medical and Dental Council¹. Some neurology training programs do not give exposure to subspecialties and training is focused on adult neurology². From 2015 to 2016, several conferences were held on neurology including an Annual Meeting in Quetta, movement disorder conference in Lahore

Plagiarism penalties

Research in all areas of sciences and humanities has led to the creation of a highly competitive environment which necessitates reporting of ideas, and discoveries at rapid pace. The emergence of new technologies of communication has significantly enhanced the capabilities of individuals to record and transcribe data at high speed. Even though, one can accumulate information in a fraction of time, but quite often the creative skills and ability to write one‘s own original thoughts do not match the required level of output. Writing ideas in one’s own words is not always easy and at times it becomes quite challenging particularly for those with limited command over the language. These situations often tempt a writer to look around easily available resources

Neurology in the 21st century: contemporary state of diagnostics and therapeutics

Although neurological disease has been recognized since antiquity, neurology as a systematic clinical discipline is less than 130 years old. Neurological practice has traditionally been constrained by the complexity of the human nervous system, which has been slow to yield its secrets. Over the last three decades, however, clinical neurology has been transformed in terms of both diagnostics and therapeutics and now marches in lockstep with the cutting edge of medicine. Efficacious treatments are now available for the majority of neurological diseases, including epilepsy, migraine, Guillain-Barre syndrome, Parkinson\u27s disease, multiple sclerosis, and ischemic stroke. This neurological revolution has been enabled by advances in neuroimaging and through the integrated application of basic research, drug development, biotechnology and clinical trial methodology. Neurology in the 21st century is a dynamic specialty offering relief and benefit to many patients, and holding the promise for one day conquering neurological disease in all its manifestations

Botulinum toxin type-A in the management of cerebral palsy: low or high dose?

Cerebral palsy is the most common cause of severe physical disability in childhood. Spasticity is a common and disabling symptom for many patients with cerebral palsy. Therapy for spasticity is symptomatic with the aim of increasing functional capacity and relieving discomfort. Spasticity treatment by orally administered drugs and intramuscular chemodenervation agents has become more frequent. Most oral medications to treat spasticity have been inadequately studied in children, especially those with cerebral palsy. Since its first use in pediatric patients, reported in 1993, botulinum toxin (BTX-A), a relatively recent addition to the available medical interventions for children with cerebral palsy, has rapidly gained acceptance as a treatment of spasticity. The clinical effects of BTX-A have been reported to include decreased spasticity and increased range of motion. However, no consensus exists among clinicians about how an optimal dose of BTX-A should be determined and there are no standard guidelines on doses of BTX-A in children. Doses of 2-6 U/kg with a maximum total dose of 29 U/kg have been reported. Although there are no standard guidelines on doses in children. The current practice is to inject BTX-A at higher doses than reported in the past. Larger dose of BTX-A is used more frequently, which isconsidered safe, more effective, and better tolerated by children. Titration of the dose of BTX-A is necessary because muscle spasticity affects different patients in different ways. The dosage of BTX-A must be individualized for each patient

Idiopathic epilepsy of childhood and potassium ion channels

Potassium can affect the development of common seizure type and can be defined seizure susceptibility allele. The existence of inward-rectifying potassium (Kir) channels was first recognized half a century ago. The biophysical fingerprint of Kir channels is inward rectification in the current-voltage relationship , which limits potassium efflux at depolarizing membrane potentials. Kir channels are essential in the control of resting membrane potential, coupling of the metabolic cellular state with membrane excitability, and maintenance of potassium homeostasis. The critical interval contains several candidate genes, one of which, KCNJ10, exhibits a potentially important polymorphism with regard to fundamental aspects of seizure susceptibility. Deletion of KCNJ10 as a seizure susceptibility gene that code for inward rectifier potassium ion channels imparts protection against seizures results in spontaneous seizures and increased seizure susceptibility. The unique role of Kir channels in membrane physiology coupled with previous strong association between ion channel gene mutations and seizure phenotypes puts even greater focus on KCNJ1

Dementia – the next impending epidemic knocking on our door – are we ready?

Late-onset dementias are life-shortening diseases of largely unknown cause. Predictions of the number of persons living with dementia by 2050 have spawned alarming headlines forecasting a “tsunami” of dementia cases that will overwhelm families and health care systems and impose unbearable economic burdens [Whalley]

Diagnosis, treatment and follow-Up in four children with biotinidase deficiency from Pakistan

Biotinidase deficiency is an inherited disorder in which the vitamin biotin is not recycled. If untreated, affected individuals develop neurological and cutaneous symptoms. Untreated individuals with biotinidase deficiency either succumb to disease or are left with significant morbidity. We describe clinical course and follow-up of 4 children from Pakistan. All 4 presented with classical symptoms of biotinidase deficiency and responded dramatically to oral biotin within days to weeks. Biotinidase deficiency is reported in Pakistani children from different part of world, however; there is no such report from Pakistan. This highlights lack of awareness of biotinidase deficiency among physicians in Pakista