Pseudoseizures or psychogenic non-epileptic seizures (PNES) are often misdiagnosed as epilepsy. This review discusses what is known about PNES, the importance of differentiating PNES from epileptic seizures (ES), avoiding iatrogenic harm and of identifying and managing the underling psychological stressors to optimise outcome. Clinical suspicion and careful history taking with witness accounts is mandatory. Supportive investigations including video-EEG (VEEG) and the utility of VEEG and provocation are discussed. Resources to diagnose and manage PNES are an issue for most countries and clinical expertise may also be lacking. VEEG is an expensive diagnostic tool and there is variable collaboration between neurology and psychiatry which will influence how patients are managed. Confounding this, is the lack of evidence for best practice in managing PNES. The prognosis for the majority of patients with PNES appears to be poor, despite a wider recognition of the problem. Well conducted studies are needed to test the different treatment options.

Most of the primary psychiatric symptoms like delusions, hallucinations, illusions, depression, mania, obsessive compulsive symptoms, aggression etc can occur in organic neurological illnesses. Neurologist should have a clear understanding as to the differentiating clinical features from organic neurological and medical causes. The present review focuses on the clinical differentiating points which can help the neurologist to exclude organic aetiology.

There is a growing body of literature, describing disorders of bone health in epilepsy. Patients with epilepsy have a higher incidence of skeletal fractures due to multiple reasons. Postmenopausal women and elderly men are particularly vulnerable to osteoporosis. A major convulsive seizure can often lead to falls and may result in fractures. Antiepileptic therapy may have seemingly contradictory effects on bone health. It can effectively reduce the incidence of major seizures and prevent the seizure related falls and fractures. However, the central nervous system effects of these drugs increase the risk of falls, especially in the vulnerable population. Long-term antiepileptic therapy may lead to a reduction in bone mineral density, with consequent increase in bone fragility. This can increase the risk for fractures with attendant high morbidity and mortality. Dual energy X-ray absorptiometry (DXA) is currently the gold standard for assessing bone mineral density. Multiple pathophysiologic mechanisms have been proposed for the reduction in bone mineral density associated with antiepileptic therapy. Most of the available data are from the patients treated with conventional antiepileptic drugs (AED). There is a need for monitoring the effects of the newer AEDs on the bone mineral metabolism. This is of added significance in view of an ageing population and also an increase in the prevalence of epilepsy in the elderly. Physicians treating patients with epilepsy should be made aware of this problem and adequate preventive measures should be advised especially in patients with multiple risk factors. A multidisciplinary approach with the help of an endocrinologist may be needed in severe bone disease.

Neurological disorders with a prolonged course, either remediable or otherwise are being seen increasingly in clinical practice and many such patients are young and are part of some organization or other wherein their services are needed if they were healthy and fit. The neurologists who are on the panel of these organizations are asked to certify whether these subjects are fit to work or how long they should be given leave. These certificates may be produced in the court of law and may be subjected to verification by another neurologist or a medical board. At present there are no standard guidelines in our country to effect such certification unlike in orthopedic specialty or in ophthalmology. The following is a beginning, based on which the neurologist can certify the neurological disability of such subjects and convey the same meaning to all neurologists across the country.

Background: The cause of sporadic motor neuron disease (MND) or amyotrophic lateral sclerosis (ALS) is unknown. During the last 20 years, at least 23 cases of MND have been reported in HIV-1 (HIV) seropositive individuals. Objective: To describe two patients with HIV infection and MND and to review the literature regarding HIV-associated MND. Setting: A multidisciplinary ALS center and Neuro-AIDS clinic at tertiary care university hospitals. Patients/Design: We prospectively studied two HIV-infected patients with motor neuron disease. A detailed review of the literature employing the PubMed search strategy revealed 23 additional cases of MND in HIV-infected persons. These were reviewed for comparison and contrast with the characteristics of sporadic classical MND. Results: The clinical features of MND in our two cases, mirrored that of the sporadic MND (upper and lower motor neuron disorder) and primary lateral sclerosis (PLS, isolated upper motor neuron disorder). The review of 23 previously reported patients with MND and HIV infection revealed that they could be categorized into clinically definite MND (6 cases) or clinically probable or possible MND (17 cases). MND commenced at different stages of the HIV; in 9 patients HIV infection was discovered contemporaneously with the diagnosis of MND. As in our one patient, 14 of 18 patients with HIV-associated MND syndrome receiving highly active antiretroviral therapy (HAART), demonstrated at least partial recovery of their motor deficit. Conclusions: A clinical picture similar to MND or PLS may occur in association with HIV infection. An aggressive HAART regimen to reduce viral load should be pursued in all such cases.

Focal muscular atrophy (FMA) can occur due to several causes. We report three cases of FMA associated with deficiency of hexosaminidase A. The serum level of hexosaminidase A was assayed in seven patients with FMA without any definite aetiology identified over a period of two years. Three cases of FMA showed deficiency of hexosaminidase A. All these patients had clinical features of isolated lower motor neurone involvement in one limb without any evidence of involvement of the rest of the neuraxis. Detailed laboratory tests were negative. Electromyography confirmed neurogenic involvement without any evidence of radiculopathy or neuropathy. Hexosaminidase deficiency as a possible association for FMA is highlighted.

We report a 19-year-old man who presented with 2 weeks history of fever, myalgia, swelling of the face and body and raised serum CK level. Following partial response to steroids, he deteriorated clinically. On admission, he had an ill look, hepatomegaly, muscle weakness and multiple, fluctuant and non-tender subcutaneous swellings of variable size, over the right forearm and left thigh. Diagnostic procedures revealed it to be tropical pyomyositis due to staphylococcus aureus. He improved completely with parenteral cloxacillin. Reporting of such cases will increase awareness.

There is a diverse clinical spectrum of peripheral nervous system involvement in Sjogren's syndrome (SS). Most of the peripheral neuropathies in SS are typically sensory. In this report, we present a case who showed signs similar to those of the Miller Fisher variant of Guillain Barre syndrome, associated with SS. The patient demonstrated a rapid improvement both clinically and electrophysiologically, after high dose intravenous immunoglobulin therapy.

Muscle involvement in leprosy is rare, but not unknown. We report an interesting case of a 59 year old gentleman who presented with icthyosis, arthralgias, fever and peripheral neuropathy, mimicking a collagen vascular disease. Histological evaluation of superficial peroneal nerve and peroneus brevis revealed unusual dual involvement by Hansen's disease, with numerous lepra bacilli in both. Involvement of skeletal muscle by Mycobacterium is very rare. The clinical presentation and treatment details of the case with a brief review of literature, is presented.

CT scan images may show fluid level in cerebral hemorrhage secondary to anticoagulation, thrombolytic therapy or with amyloid angiopathy. Other causes of fluid levels are cerebral hemorrhage with underlying malignancy, cerebral arteriovenous malformations or radiation. We are reporting a putaminal hemorrhage with fluid level in a patient with high blood pressure. This case was unusual in the absence of any of these factors and rare location in the putamen.