Sleep disturbance in multiple sclerosis: correlation with clinical and MRI findings

Sleep disorders are pervasive in patients with multiple sclerosis [MS], although clinically under recognized by most physicians. Approximately half of all patients with MS report sleep-related problems. To determine whether disturbance of sleep exists in patient with MS and if they correlate with clinical and magnetic resonance imaging [MRI]. We studied twenty two patients with MS. They were subjected to full clinical and neurological assessment, sleep history, an overnight and on the following day polysomnographic [PSG] study, and MRI study. Fifteen healthy subjects were selected as a control group. MS patients had significantly reduced sleep efficiency, remarkable increased in sleep latency and arousal index, decreased depth of sleep, increased PLM index and respiratory disturbance index [RDI], and decreased REM sleep percentages. Factors that influence quality of sleep in those patients were studied. Sleep disturbances are pervasive in patients with MS, they may be due to physical discomfort, disease severity, nocturia, pain, nocturnal movement disorder, sleep- disordered breathing, location of lesion and narcolepsy

Sleep disordered breathing in different endocrinal diseases

Sleep-disordered breathing [SDB] is an extremely common condition that compromises the vital functions of respiration and circulation. As currently defined, obstructive sleep apnea [OSA] is associated with considerable morbidity and mortality, whereas the currently available treatments are associated with either limited efficacy and/or poor compliance. An improvement in the understanding of the nature and pathophysiology of the disorder may lead to novel treatments. The objectives of the present study are to detect apnea /hypopnea as an indicator of SDB in patients with some endocrinal diseases, namely diabetes mellitus, hypothyroidism, acromegaly and Cushing for early management and better quality of life. We studied sixty-five patients with different endocrinal diseases [group A]. They were further subdivided into: group 1 [25 patients with diabetes mellitus], group 2 [16 patients with hypothyroidism], group 3 [12 patients with acromegaly] and group 4 [12 patients with Cushing disease]. All groups were subjected to full clinical and neurological assessment, sleep history, laboratory investigations, and an overnight polysomnographic [PSG] study. Twenty healthy subjects were selected as a control group [group B]. Respiratory disturbance index [RDI] was significantly higher in all patients groups compared to control group. HbA1c, FBS, as well as 2hr PP correlated positively with RDI in group [1]. No significant correlation was observed between RDI and serum TSH, T3 and T4 levels in group [2]. Acromegalic patients with SDB had significantly higher growth hormone [GH] level which correlated positively with RDI in group [3]. No significant correlation was observed between RDI, serum ACTH and 24 hours urinary cortisol levels in group [4]. There are complex interactions between OSA and neuroendocrine function. Understanding this complex relation may lead to more effective, better tolerated treatment for sleepiness and SDB. It is increasingly important that in patients presented to sleep laboratory, careful medical evaluation should be done to all cases presented with sleepiness and had manifestation of sleep apnea to exclude different endocrinal diseases

Clinically unapparent central nervous system impairment in diabetic patients

Diabetes mellitus is the result of absolute or relative hypoinsulinemia, and is currently described as an endocrine disease that causes damage to many organs and systems. The consequences of chronic diabetes mellitus in the central nervous system [CNS] are less known than diabetic peripheral neuropathy and autonomic nervous system neuropathy. Damage to the brain and the spinal cord is less common. is to show the importance of motor and somatosensory evoked potentials [MEP and SEP] for the early diagnosis of unapparent CNS damage related to diabetes mellitus. Thirty diabetic patients [type 1 and type 2] and twenty healthy volunteers who match patient group for age and sex, both groups with no clinical symptoms or signs of central or peripheral nervous system lesion were evaluated. MEPs were recorded from upper and lower extremities bilaterally and central motor conduction time [CMCT] was calculated according to formula: CMCT=MEP-[0.5x [F-M-1] +M]. Similarly, we examined spinal and cortical SEP after median nerve stimulation in diabetics and control group. We measured the peak latencies of individual wave deflections and peripheral and central conduction time of spinal and cortical SEP. The examination of MEPs and SEPs proved and confirmed the prolongation not only of peripheral conduction time, but also of the central conduction time especially in the lower limbs in the diabetic patients compared to the control group. There was no correlation between central conduction time delay and the degree of metabolic control, type of diabetes [type 1 or type 2 diabetes mellitus], patient age, disease duration, presence or absence of retinopathy or nephropathy. In spite of an absence of clinical signs of central nervous system lesion in diabetic patients, a significant prolongation of central conduction time compared to control group was recorded. We assume a presence of diffuse subclinical CNS lesion induced by many factors. Measurement of central conduction time using transcranial magnetic stimulation and somatosensory evoked potentials could be a complementary electrophysiological method for assessment of subclincal cerebral and spinal cord involvement in diabetic patient