BackgroundDisordered sleep breathing is a common complication of diabetic peripheral neuropathy (DPN) manifested by excessive daytime sleepiness, morning headache, morning dizziness, cognitive decline, and mood changes.MethodsThis study was performed on 30 non-obese type 2 diabetic patients; 20 with clinically evident DPN and 10 without. Ten age-, sex-, and body mass index-matched healthy control subjects were also included. Patients and control were subjected to history taking, neurological examination, glycated hemoglobin, and clinical assessment of the sensori-motor manifestations by the neuropathy symptom score and neuropathy disability score. The autonomic nervous system was evaluated clinically by the systolic blood pressure response to standing and heart rate response to each of standing, Valsalva, and deep breath. Finally, sleep was assessed by one-night polysomnogram (PSG) followed by multiple sleep latency test in the next day.ResultsThe study showed significant increase in sleep apnea syndromes in diabetic peripheral neuropathy patients compared to diabetic neuropathy free patients and healthy control (p < 0.0001). The sleep apnea was mainly obstructive and to a little extent mixed (obstructive/central) sleep apnea. The severity of sleep PSG abnormalities was positively correlated with the severities of sensory, motor, and autonomic manifestations.ConclusionsNon-obese type 2 diabetic patients complicated by peripheral neuropathy especially those having dysautonomia are at increased risk of developing sleep disordered breathing resulting in their excessive daytime sleepiness, decreased productivity, and poor glycemic control.

Pesticide exposure is associated with increased risk of Parkinson’s disease (PD). We investigated in Egypt whether common variants in genes involved in pesticide detoxification or transport might modify the risk of PD evoked by pesticide exposure. We recruited 416 PD patients and 445 controls. Information on environmental factors was collected by questionnaire-based structured interviews. Candidate single-nucleotide polymorphisms (SNPs) in 15 pesticide-related genes were genotyped. We analyzed the influence of environmental factors and SNPs as well as the interaction of pesticide exposure and SNPs on the risk of PD. The risk of PD was reduced by coffee consumption [OR = 0.63, 95% CI: 0.43–0.90, P = 0.013] and increased by pesticide exposure [OR = 7.09, 95% CI: 1.12–44.01, P = 0.036]. The SNP rs1126680 in the butyrylcholinesterase gene BCHE reduced the risk of PD irrespective of pesticide exposure [OR = 0.38, 95% CI: 0.20–0.70, P = 0.002]. The SNP rs1803274, defining K-variant BCHE, interacted significantly with pesticide exposure (P = 0.007) and increased the risk of PD only in pesticide-exposed individuals [OR = 2.49, 95% CI: 1.50–4.19, P = 0.0005]. The K-variant BCHE reduces serum activity of butyrylcholinesterase, a known bioscavenger for pesticides. Individuals with K-variant BCHE appear to have an increased risk for PD when exposed to pesticides.

Background: Nocturnal enuresis (NE) is a very common chronic pediatric problem with bad psychological consequences. Methods: Forty primary monosymptomatic nocturnal enuresis (MNE) children and 20 healthy controls were recruited in the study and subjected to history taking, neurological and urological examinations, and psychological assessment using the Arabic-translated and validated version of child behavior checklist, sleep architecture studying through onenight polysomnography (PSG), and vasopressin levels determination both diurnal and nocturnal. Results: Enuretic children had positive family history of NE in 42.5%, inverted vasopressin circadian rhythm in 52.5% and PSG changes in the form of increased N3 deep sleep % of total sleep time (TST), sleep stage transition index (SSTI), periodic limb movement index (PLMI), and snore index. Enuretic children PSG showed decreased deep sleep latency, N1% of TST, N2% of TST, and REM % of TST. The child behavior checklist showed higher anxious depressed symptoms, social problem, attention problems, and internalizing problems in enuretic children than control subjects. Conclusions: MNE is a heterogeneous disorder with multiple factors interplay in its pathogenesis. So, the management must be tailored patient by patient according to the dominating etiology.

Background Olfactory dysfunction (OD) is a well-established nonmotor manifestations (NMM) of Parkinson disease (PD) which needs objective assessment for better understanding of the disease pathogenesis. The aim of this work was quantitative and qualitative assessment of olfactory performance in newly diagnosed PD patients. Methods This study was performed on 32 recently diagnosed PD patients and 24 healthy controls subjects (HCS) submitted to unified Parkinson’s disease rating scale–III (UPDRS–III), extended n-butanol Sniffin’ Sticks test (SST) and olfactory bulbs volumetry (OBV). Results There were significant decreases in SST threshold, discrimination, identification, and TDI variables as well as OBV in PD patients compared to HCS. The olfactory performance was negatively correlated with disease duration but had no relation with PD severity as well as motor subtype. Conclusion OD is highly prevalent during the early stages of PD which is both measurable and specific with identification and discrimination impairments to certain odors which makes smell performance testing an important step in PD patients’ evaluation.

Alzheimer's disease (AD) is the most common type of dementia and the most common neurodegenerative disorder of elderly. It is not an accelerated form of aging but it is characterized by distinct temporospatial brain pathological changes, including amyloid plaques accumulation, neurofibrillary tangles deposition, synaptic loss and neuronal death with gross brain atrophy. These changes result in persistent progressive memory and cognitive decline interfering with the usual daily activities. AD is a multifactorial disorder results from the interaction of genetic, epigenetic, environmental and lifestyle factors. Estrogen, progesterone and androgen effects are important building stones in AD pathogenesis, and their effect in brain modulation and development results in different gender susceptibility to the disease. These sex hormones whether gonadal or neurosteroids (synthesized locally in the brain) play important neuroprotective roles influencing the individual's vulnerability to AD development, rate of mild cognitive impairment (MCI)/AD conversion and speed of AD progression. Despite the little therapeutic implications of hormonal replacement therapy in AD treatment, yet this topic still represents a challenging hopeful way to construct a strategy for the development of personalized, gender-specific AD management.

Background Essential tremor (ET) is now considered as a slowly progressive neurodegenerative disorder with a variety of motor and non-motor manifestations. The objectives of this work were to study the existence of cognitive, mood, olfactory, and balance dysfunctions in ET patients and their relation to tremor severity as well as patients’ activity of daily livings. Methods This study was performed on 36 ET patients and 24 healthy controls subjects (HCS) submitted to The Essential Tremor Rating Assessment Scale (TETRAS), advanced activity of daily living scale (AADLs), Montreal cognitive assessment scale (MoCA), Montgomery–Åsberg Depression Rating Scale (MADRS), auditory mismatch negativity (MMN), Sniffin’ Sticks test (SST), computerized dynamic posturography (CDP), and brain MRI diffusion tensor tractography (DTT). Results ET patients showed significant decrease in AADLs, MoCA, SST (threshold, identification, and discrimination subscales) as well as visual and vestibular ratios of CDP compared to HCS. Auditory MMN showed significant reduction in the amplitude and prolongation of latencies while corticospinal tracts, thalamo-cortical connectivity, and middle cerebellar peduncles DTT revealed reduced fractional anisotropy in ET patients with normal tracts densities. Conclusion ET patients exhibit a wide variety of non-motor manifestations including cognitive impairment, depressive symptoms, hyposmia, and increased risk of falls with consecutive reduced activity of daily living beyond the deleterious effects of the kinetic tremor.

Introduction: Autoimmune epilepsy was an under-recognized condition, and its true incidence was unknown in pediatrics. Serum antibodies suggesting a potential autoimmune etiology were detected in 34.8% of patients presented by epilepsy of unknown etiology. Diagnosis of autoimmune epilepsy would be of great value in the search for potential preventive treatments for disabling seizures and cognitive impairment. Autoimmune epilepsy was characterized by a depressed or altered level of consciousness, lasting more than 24 h, lethargy, or change in personality or behavior and at least one of the following features: neuropsychiatric symptoms, seizures, movement disorder, or cognitive dysfunction. Patients were excluded if an alternative diagnosis was made. The presence of neuronal antibodies and MRI changes supported the diagnosis. This study aimed to assess the possible role of immunity in the pathogenesis of pediatric drug resistant epilepsy through clinical electroencephalographic, neuroimaging and neuro-immunological testing. Subjects and Methods: This study was conducted on twenty-four drug resistant epileptic children with suspected autoimmune etiology over the period from 2016-2018. The control group comprised twenty four children with idiopathic controlled epilepsy matched to the drug-resistant epilepsy sample for age and gender. Both groups were subjected to clinical examination, neuronal antibodies in serum and CSF, Mini-Mental State Examination (MMSE), Chalfont seizure severity scale (CSSS), EEG, and brain MRI studies. Results: There was a large percentage of autoimmune epilepsy in pediatric cryptogenic drug-resistant epilepsy. 55% of DRE cases presented with mild pleocytosis and elevated CSF proteins. Serum and CSF neuronal antibodies were positive in about 66.63% and 65% of cases respectively. Serum neuronal antibodies to GAD were positive in 8.33%, NMDA Abs were positive in 33.3%, and VGKC Abs were in 25.0% of cases. In the CSF, GAD antibodies were positive in 10%, NMDA antibodies in 40%, and VGKC antibodies in 20% of cases. Seizures reduction was achieved with immunotherapy, also was prevalent in seropositive cases. Conclusion: Pediatric patients presented by drug-resistant epilepsy should receive immunotherapy for a definite diagnosis. MRI changes in the form of temporal hyperintensity, claustrum, cortical hyperintensities were a common finding in pediatric patients presented by drug-resistant epilepsy. CSF changes in the form of elevated proteins and /or mild pleocytosis signified inflammatory changes in the CNS and blood brain barrier (BBB) disruption. Steroid responsiveness played a major role in the diagnosis of autoimmune epilepsy, especially seronegative cases.