Tag: weakness

Truncal ataxia or disequilibrium is an unrecognised cause of orthostatic intolerance in patients with myalgic encephalomyelitis

Introduction:

Chronic fatigue syndrome (CFS) causes a marked reduction in the activities of daily living and impairs the quality of life. Recently, dysfunction of the central nervous system associated with myalgic encephalomyelitis (ME) has been postulated as the main cause of CFS.1 Most patients with ME/CFS have orthostatic intolerance (OI) which is the primary factor restricting the daily functional capacity and in turn quality of life.2-4 OI is characterised by the inability to remain upright without severe signs and symptoms, such as hypotension, tachycardia, light-headedness, pallor, fatigue, weakness, dizziness, diminished concentration, tremulousness and nausea. Most symptoms of OI have been surmised to be related to reduced cerebral blood flow with or without impaired cerebral circulatory autoregulation, and the compensatory activation of the sympathetic nervous system.5, 6 Indeed, many patients have postural orthostatic tachycardia, delayed orthostatic hypotension and neurally mediated hypotension.4, 5, 7-9 Also many patients have low cardiac output in association with a small left ventricle.10-12 With further progression of the disease, patients may have even sitting intolerance and finally become bedridden.

Although static balance is an essential element for the performance of daily activities as well as postural stability, the possible relation between disequilibrium and OI has never been investigated. The possible role of static or truncal ataxia in the genesis of both orthostatic and sitting intolerance was examined in patients with ME.

Source: Miwa K, Inoue Y. Truncal ataxia or disequilibrium is an unrecognised cause of orthostatic intolerance in patients with myalgic encephalomyelitis. Int J Clin Pract. 2017 Jun;71(6). doi: 10.1111/ijcp.12967. PMID: 28613452. https://onlinelibrary.wiley.com/doi/10.1111/ijcp.12967 (Full text)

The link between idiopathic intracranial hypertension, fibromyalgia, and chronic fatigue syndrome: exploration of a shared pathophysiology

Abstract:

PURPOSE: Idiopathic intracranial hypertension (IICH) is a condition characterized by raised intracranial pressure (ICP), and its diagnosis is established when the opening pressure measured during a lumbar puncture is elevated >20 cm H2O in nonobese patients or >25 cm H2O in obese patients. Papilledema is caused by forced filling of the optic nerve sheath with cerebrospinal fluid (CSF). Other common but underappreciated symptoms of IICH are neck pain, back pain, and radicular pain in the arms and legs resulting from associated increased spinal pressure and forced filling of the spinal nerves with CSF. Widespread pain and also several other characteristics of IICH share notable similarities with characteristics of fibromyalgia (FM) and chronic fatigue syndrome (CFS), two overlapping chronic pain conditions. The aim of this review was to compare literature data regarding the characteristics of IICH, FM, and CFS and to link the shared data to an apparent underlying physiopathology, that is, increased ICP.

METHODS: Data in the literature regarding these three conditions were compared and linked to the hypothesis of the shared underlying physiopathology of increased cerebrospinal pressure.

RESULTS: The shared characteristics of IICH, FM, and CFS that can be caused by increased ICP include headaches, fatigue, cognitive impairment, loss of gray matter, involvement of cranial nerves, and overload of the lymphatic olfactory pathway. Increased pressure in the spinal canal and in peripheral nerve root sheaths causes widespread pain, weakness in the arms and legs, walking difficulties (ataxia), and bladder, bowel, and sphincter symptoms. Additionally, IICH, FM, and CFS are frequently associated with sympathetic overactivity symptoms and obesity. These conditions share a strong female predominance and are frequently associated with Ehlers-Danlos syndrome.

CONCLUSION: IICH, FM, and CFS share a large variety of symptoms that might all be explained by the same pathophysiology of increased cerebrospinal pressure.

Source: Hulens M, Rasschaert R, Vansant G, Stalmans I, Bruyninckx F, Dankaerts. The link between idiopathic intracranial hypertension, fibromyalgia, and chronic fatigue syndrome: exploration of a shared pathophysiology. J Pain Res. 2018 Dec 10;11:3129-3140. doi: 10.2147/JPR.S186878. eCollection 2018. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6292399/ (Full article)

Decreased immunoreactive beta-endorphin in mononuclear leucocytes from patients with chronic fatigue syndrome

Abstract:

OBJECTIVE: To investigate beta-endorphin concentrations in the peripheral blood mononuclear cells (PBMC) of patients with chronic fatigue syndrome (CFS).

METHODS: Sixteen patients with CFS were enrolled in this study. Ten healthy subjects were studied as controls. Beta-endorphin concentrations were measured in PBMC by radioimmunoassay performed with antibodies specific for the C-terminal portion of human beta-endorphin.

RESULTS: Beta-endorphin concentrations in the PBMC of chronic fatigue patients were significantly lower (p < 0.001) than in healthy subjects (mean +/- SD: 8.5 +/- 7.0 vs. 42.6 +/- 22.6).

CONCLUSION: Patients with CFS were found to have low levels of PBMC beta-endorphin. This finding may reflect the condition of chronic immune activation in CFS that has been reported in previous investigations. Beta-endorphin concentrations in PBMC seem to mirror the central nervous system homeostasis of the opioid. Therefore, we would postulate that the fatigue and weakness typical of CFS could be related to low beta-endorphin concentrations at the central nervous system level.

 

Source: Conti F, Pittoni V, Sacerdote P, Priori R, Meroni PL, Valesini G. Decreased immunoreactive beta-endorphin in mononuclear leucocytes from patients with chronic fatigue syndrome. Clin Exp Rheumatol. 1998 Nov-Dec;16(6):729-32. http://www.ncbi.nlm.nih.gov/pubmed/9844768