Pratap Chand

Multifactorial sleep disturbance in Parkinson's disease

Parkinsons disease (PD) is the second most common neurodegenerative disorder, ranking only behind Alzheimers disease and affecting 2% of the population over the age of 65. Pathophysiologically, PD is characterized by selective degeneration of the dopaminergic neurons of the substantia nigra pars compacta (SNpc) and striatal dopamine depletion. Patients may also exhibit mild-to-severe degeneration of other central and peripheral nervous tissues. The most dramatic symptoms of the disease are profound dopamine-responsive motor disturbances, including bradykinesia, akinesia, rigidity, resting tremor, and postural instability. PD patients commonly present with debilitating non-motor symptoms, including cognitive impairment, autonomic nervous system dysfunction, and sleep disturbance. Of these, sleep disturbance is the most consistently reported, and likely represents a disorder integrative of PD-related motor impairment, autonomic nervous system dysfunction, iatrogenic insult, and central neurodegeneration. The pathophysiology of PD may also indirectly disrupt sleep by increasing susceptibility to sleep disorders, including sleep disordered breathing, periodic limb movements, and REM behavior disorder. In this review, we will discuss these systems representing a multifactorial etiology in PD sleep disturbance.

Abnormalities of nerve conduction and somatosensory evoked potential in Poland's syndrome.

Summary We report a case of Polands dyndrome with associated primary generalized tonic-clonic epilepsy. Somatosensory evoked potentials at median nerve stimulation showed delayed latencies and reduced amplitudes of the evoked response from the hypoplastic right upper limb. Nerve conduction studies showed reduced mixed nerve conduction velocity in the right ulnar nerve and decrease in amplitudes of the compound nerve action potentials in the right median and ulnar nerves. We postulate a congenital hypoplasea of the above nerves and brachial plexus in the present case.

Segmental ballism due to acute ischemic lesions of the caudate nucleus and parietal lobe: Case report and review of the literature

Ballism is a relatively rare hyperkinetic movement disorder with very low incidence at about 1 in 500,000 in the general populaion [1,2]. It is characterised by irregular, wide amplitude, vigorous, oorly patterned movements of the limbs, primarily due to activity f the proximal limb and associated axial muscles [1]. The moveents are usually continuous but may be intermittent and can e voluntarily suppressed by the patient, although only for a few inutes. They are most prominent during periods of rest but are bsent during sleep. In some patients, the movements are so severe hat they lead to physical exhaustion or injury of the affected limb rom striking bedrails and walls [3]. Ballism can occur in associaion with other types of involuntary movements, such as dystonia, yoclonus, or orofacial gestures [4]. The ballistic movements can ppear in one limb “monoballism”, involve the entire side of the ody including the face “hemiballism”. When both sides of the body re affected, it is termed “biballism” or “paraballism” [2,5]. Hemiballism is sometimes used interchangeably but distinuished from hemichorea by the fact that hemichoreic movements re slower, more randomly distributed, less violent, and involve ore of the distal musculature [3]. Some patients with hemiballism lso have choreiform movements; therefore, the “hemiballismemichorea” is used to describe this clinical spectrum [3,6,7]. Hemiballism was thought as pathognomonic of a lesion in the ubthalamic nucleus (STN). The prognosis was described as grave,

Corrigendum to “Multifactorial sleep disturbance in Parkinson's disease” [Sleep Med 35 (2017) 41–48]

Corrigendum to “Multifactorial sleep disturbance in Parkinsons disease” [Sleep Med 35 (2017) 41e48] J. Andrew Albers a, c, , Pratap Chand a, , A. Michael Anch c a Saint Louis University School of Medicine, 1402 South Grand Blvd, St Louis, MO 63104, United States b Department of Neurology and Psychiatry, Saint Louis University School of Medicine, Monteleone Hall, 1438 South Grand Blvd, St Louis, MO 63104, United States c Department of Psychology, Saint Louis University College of Arts and Sciences, Morrissey Hall, 3700 Lindell Blvd, St Louis, MO 63108, United States

Chemical Leukoderma: A Rare Adverse Effect of the Rotigotine Patch

Rotigotine, marketed as Neupro, is a non-ergot dopamine agonist (DA) available as a transdermal therapeutic system (TTS).1 It was approved in 2007 for Parkinsons disease (PD)2 and in 2008 for Restless Leg Syndrome.3 It has high affinity for the D3/D2/D1 receptors.1 The TTS gives Rotigotine the advantage of direct entry into the systemic circulation bypassing the intestinal absorption and the first pass liver metabolism with stable plasma concentration leading to uniform symptomatic control. It is available in six different strengths in the market ranging from 1mg/24hr to 8 mg/24hr. This article is protected by copyright. All rights reserved.

Mixed Clinical Response After Total Thyroidectomy in Two Patients with Hashimoto's Encephalopathy

Importance: Hashimoto’s encephalopathy (HE) is currently treated with medical therapy. Only one case of thyroidectomy as treatment for HE has been presented in the literature. We present two patients with distinct manifestations of (HE) who underwent thyroidectomy after minimal response to medical management. Observations: Patient 1 is a 71 year-old female who presented with motor restlessness. She had persistently elevated antithyroid antibodies. After thyroidectomy, her symptoms were only mildly improved. Iodine-123 thyroid scan revealed a small remnant of thyroid tissue. Her antithyroid antibodies remained elevated. Patient 2 is a 60 year-old female with previous diagnosis of (HE) who presented with recurrent seizures. She had a history of elevated antithyroid antibodies. After thyroidectomy, she no longer had seizures, and her antithyroid antibodies normalized. Conclusions and relevance: Patient 1 did not improve as quickly as patient 2. A possible explanation for this is the thyroid tissue remnant found in the first patient during a follow-up iodine-123 thyroid scan; the remnant could be responsible for persistently elevated antithyroid antibodies. The degree or pattern of preoperative antithyroid antibody elevation does not seem to be predictive of postoperative response. Thyroidectomy is a reasonable treatment option for the severely symptomatic patient who has failed medical therapy with steroids, IVIG, and plasmapharesis.

Parkinson’s Disease: An Overview of Pathogenesis

Parkinson’s disease (PD) is clinically, pathologically, and etiologically diverse and complex combinations of genetic susceptibility and environmental risk factors like age, gender, estrogen status, race/ethnicity, exposure to pesticides, and head trauma play roles in the pathogenesis. Genetic research has identified eleven PARK loci in familial cases and genotyping technology has allowed genome-wide approaches in large populations of patients with sporadic PD. Neuropathologic studies have defined and characterized more than 30 proteins with the core filament of α-synuclein in the Lewy body inclusions of idiopathic PD. Analysis of Lewy body pathology has outlined progressive disease stages in which the intracellular deposition of α-synuclein affects medullary sites before more rostral brain regions and the late stages of involvement of cortical association neurons. In PD, there is evidence of protein misfolding, aggregation, and abnormal neuronal apoptosis. Toxin-based and recent gene mutation-based animal models of PD in mammals, flies, fish, and worms have reproduced the progressive motor and non-motor deficits observed in PD patients and shown dopamine dysfunction and delayed loss of dopaminergic neurons in the substantia nigra. Oxidative stress plays a key role in the pathogenesis of PD and the demonstration of nitrated protein within Lewy bodies and neurites provides evidence of oxidative damage in the pathogenesis of PD. Reduction in the mitochondrial enzyme complex I in PD renders neurons vulnerable to unstable oxygen free radicals and causes alpha-synuclein to aggregate into fibrils and lead to dopaminergic neuronal loss. The DJ-1 gene has antioxidant function in the cellular response to oxidative stimuli and DJ-1 is oxidatively damaged in the brains of PD patients. The occurrence of a parkinsonian syndrome in families with mutations in the DJ-1 gene also supports a role for oxidative stress in the pathogenesis of PD. Therapeutic approaches that could prevent or limit oxidative reactions in PD represent a viable strategy for the development of newer antiparkinsonian drugs.