Lamotrigine Induced Dystonia in a Patient with Bipolar Affective Disorder

Bipolar disorder, formerly manic depression, is a mental disorder with periods of depression and periods of elevated mood. The elevated mood is significant and is known as mania or hypomania, depending on its severity, or whether symptoms of psychosis are present. During mania an individual behaves or feels abnormally energetic, happy or irritable. 

Individuals often make poorly thought out decisions with little regard to the consequences. The need for sleep is usually reduced during manic phases. During periods of depression there may be crying, a negative outlook on life, and poor eye contact with others. The risk of suicide among those with the illness is high at greater than 6 percent over20 years, while self-harm occurs in 30-40 percent. Other mental health issues such as anxiety disorders and substance use disorder are commonly associated.

The causes are not clearly understood, but both environmental and genetic factors play a role. Many genes of small effect, contribute to risk. Environmental factors include a history of childhood abuse and long-term stress. It is divided into bipolar I disorder if there is at least one manic episode and bipolar II disorder if there are at least one hypomanic episode and one major depressive episode. In those with less severe symptoms of a prolonged duration the condition cyclothymic disorder may be present. If due to drugs or medical problems it is classified separately. Other 

conditions that may present in a similar manner include attention deficit hyperactivity disorder, personality disorders, schizophrenia and substance use disorder as well as a number of medical conditions. Medical testing is not required for a diagnosis. However, blood tests or medical imaging can be done to rule out other problems.

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Neuroplasticity in Treatment of Schizophrenia

Neuroplasticity is pointed to the ability of the brain to change its molecular and structural characteristics that hinder its function. The main pathophysiological alteration in schizophrenic patients is the occurrence of a major deficit in cognitive process that is under the control of the circuitry of the dorsolateral prefrontal cortex (DLPFC). Additionally, this cognitive deficit inschizophrenia is partially related to the marked decrease in dopamine [DA]input to the DLPFC. However and fortunately, a compensatory response in the form of up-regulation of D1 receptor in this area of brain results in a great improvement of memory-related DLPFC activity.

Studies performed by Elvevag, Goldberg  and Black assumed that schizophrenic patients suffered from brain atrophy, neurotoxicity, or neurodegeneration that involved loss of neurons in the gray matter. Additionally, the reduction in brain volume was due to shrinkage of the neuropil surrounding the neurons with marked reduction in dendrite length that was associated with a reduction in the number and size of dendritic extensions.

This disorder is related to an alteration in the functional activity of the dorsolateral prefrontal cortex (DLPFC). DLPFC is a brain region that is related to thecontrol of executive function. Any abnormalities in the function of DLPFC are strongly related to the development and progress of schizophrenic symptoms.

Glucan from Food Supplement to a Licensed Drug

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Natural products, useful in preventing or treating various diseases, have been sought after throughout the history of humankind. Often, these molecules suffer from the same problem - these substances usuallyrepresent a complex mixture of ingredients, each of which might contribute to biological activity. These problems, together with difficulties in patenting the isolation, usually leads to lack of interest and natural molecules are left in the area of food supplements.

However, β(1-3),(1-6)-d-glucan (hereafter β-glucan), arguably the most studied natural immunomodulator, offers a different story. The original studies of effects β-glucan has on the immune system focusedentirely on mice. Subsequent studies demonstrated that β-glucan possesses a significant immunostimulating activity in a wide variety of species, including earthworms, shrimp, fish, chicken, rats, rabbits, guinea pigs, sheep, pigs, cattle, and, last but not least, humans. Based on these results, it has been concluded that β-glucan represents a type of immunostimulanting molecule that is actively spanning full evolutionary spectrum. Some experiments also show that β-glucan can help even in the protection of plants. β-Glucan is therefore not only a biologically active polysaccharide with strong immunomodulating effects, but is also considered to be an evolutionary very old stimulant of a variety of defense immune reactions.

The Diabetic Brain and Dementia

Alzheimer’s Disease (AD) and Diabetes Mellitus (DM) are the two most common and devastating health problems in the elderly. They share a number of common features among which are important impact on quality of life and substantial health care costs. Epidemiological and biological evidence support a pathophysiological link between Type 2 Diabetes Mellitus (DMT2) and cognitive impairment. A causative association between DM and Alzheimer’s disease has been suggested on the basis of clinical, epidemiological, genetic and experimental studies. Persons with DM have a higher incidence of cognitive decline and an increased risk of developing AD and other types of dementia, and comorbidity increases the risk. Insulin resistance predicts medial temporal hypermetabolism in Mild Cognitive Impairment (MCI) conversion to AD and glucose uptake changes in AD in medial temporal regions predicting worse memory performance. DM has been shown to influence the rate of functional decline among patients with mild AD dementia than in those without comorbid DM. However, the precise mechanisms involved in the development of AD in diabetics are not yet fully understood, and several pathogenic pathways have been discussed.

Autopsy studies stated that diabetic patients show significantly less AD pathology (senile plaques, neurofibrillary tangles, cerebral amyloid angiopathy, etc.) but more cerebrovascular lesions including microvascular lesions and white matter changes than subjects without DM. Vasculo-neural dysfunction has been suggested to represent a potential etiological linkage between DMT2 and AD, while others suggested that the association between DM and dementia is only partially mediated through cerebrovascular disease and that DM is associated independently with overal dementia among elderly, but not with AD or vascular dementia.

Transcranial Magnetic Stimulation in Alzheimers Disease and Cortical Dementias

Alzheimer’s disease (AD), Dementia with Lewy Bodies (DLB), Parkinson’s disease dementia (PDD) and frontotemporal lobar degeneration (FTLD), account for the predominant cause of dementia in the population aged ≥ 60 years, with an estimated prevalence of 5-7% in this age-group, escalating to about 30% in the people older than 85. With the progressive aging of the population, the prevalence of dementia is estimated to double every 20 years, thus becoming a health- and social-care priority for many high-income countries. Numerous studies have tried to addressthe challenge of identifying early biological or neuroimaging markers in order to unravel the physiopathological processes underlying these disorders and to correctly recognize the earliest stages of disease, when the neurodegenerative process is still limited and possibly reversible.

In this view, also neurophysiological techniques, particularly transcranial magnetic stimulation (TMS), have become promising tools to assess specific cortical circuits in the central nervous system. Since its introduction, the use of TMS in clinical neurophysiology, neurology, neuroscience, and psychiatry has spread widely, leading to important findings on cortical function in physiological and pathological conditions.Indeed, with the contribution of pharmacological studies, numerous TMS stimulation paradigms have been developed to assess,non-invasively and in-vivo, the function of GABAergic, glutamatergic and cholinergic cortical circuits [6]. Furthermore, specific paradigms of paired associative stimulation (PAS) or repetitive TMS (rTMS) have shown to increase or decrease the excitability of corticospinal projections of the primary motor cortex (M1), representing a form of long-term potentiation (LTP) or depression (LTD) and thus a method of assessing synaptic plasticity.

Hallermann Streiff Syndrome-The Oral Manifestations in a Child

Hallermann-Streiff-François (HSF) syndrome is marked by a characteristic facies with hypoplastic mandible and beaked nose, proportionate short stature, hypotrichosis, microphthalmia with congenital cataract, hypodontia, hypotrichosis, skin atrophy of the face and hypoplasia of the clavicles and ribs. About 15% of cases display intellectual deficit. Neonatal teeth may be present. Upper airway obstruction may result from small nares and glossoptosis (tongue falling backwards) secondary to micrognathia, and these may lead to cor pulmonale .

Tracheomalacia is a complication that can lead to chronic respiratory insufficiency, resulting in biventricular cardiac failure and early death. It is a rare clinical entity of unknown etiology that affects growth, cranial development, hair growth, and dental development . It is probably due to a developmental disorder in the 5th-6th gestational week that results in an asymmetric second branchial arch defect. Most cases are sporadic but some have mutations in the GJA1 gene (6q21-q23.2). Both autosomal dominant and autosomal recessive inheritance have been postulated. Reproductive fitness may be low but rare affected individuals have had affected offspring. Males and females are equally affected. The facies are sometimes described as ‘bird-like’ with a beaked nose. HSS is characterized by seven essential signs, as described by Francois: Dyscephaly (scaphocephaly or brachycephaly with frontal bossing) and typical facies (micrognathia, condylar aplasia, and thin pointed nose); dental anomalies; proportionate nanism; hypotrichosis; atrophy of the skin localized to the head and nose; bilateral microphthalmia; and congenital cataracts. It is known that the dental abnormalities are present in 50%- 80% of the cases; these abnormalities include malocclusion; open bite; severe caries; enamel hypoplasia; supernumerary and neonatal teeth; hypodontia; premature eruption of primary teeth; agenesis of permanent teeth; and maxillary hypoplasia, with poor development of the paranasal sinuses. Our main objective here is to report a case of HSS in 9 years old female child with physical and oral features consistent with the syndrome as well as detection of mutism in this child which has not been reported earlier in cases of HSS.