Category: Neurology

Neuroimaging in chronic fatigue syndrome

Abstract:

The diagnosis of chronic fatigue syndrome (CFS) is made difficult by the absence of specific biomedical markers, and depends primarily on determining whether subjective information provided by the patient meets the clinical case definition of this syndrome. Reported cognitive difficulties and/or complaints of headache may instigate referral for brain imaging.

This article will discuss the value of neuroimaging in evaluating CFS, specifically reviewing studies that (1) used static magnetic resonance imaging (MRI) to assess structural abnormalities; and (2) assessed regional cerebral blood flow (rCBF) via detection of Tc-99m hexamethylpropyl-eneamine oxime distribution by single-photon emission computed tomography (SPECT). Future research design considerations are explored including (1) the utilization of positron emission tomography (PET) and other emerging neuroimaging technologies; and (2) methodological concerns, i.e., the influence of psychopathology (such as depression) and neurologic disease (such as multiple sclerosis) as possible confounding factors.

 

Source: Lange G, Wang S, DeLuca J, Natelson BH. Neuroimaging in chronic fatigue syndrome. Am J Med. 1998 Sep 28;105(3A):50S-53S. http://www.ncbi.nlm.nih.gov/pubmed/9790482

 

Autonomic testing in patients with chronic fatigue syndrome

Abstract:

The purpose of this study was to determine whether chronic fatigue syndrome (CFS) patients show autonomic dysfunction at the cardiac level and if so, to discover whether these abnormalities explain the fatiguability and/or other symptoms in CFS.

The study population consisted of 21 CFS patients (Centers for Disease Control and Prevention [CDC] criteria, 1988) and 13 age- and sex-matched healthy controls. The autonomic testing consisted of: (1) postural challenge: registration of heart rate and blood pressure (BP) and heart rate variability in supine and in upright position (tilted to 70 degrees); (2) Valsalva maneuver; (3) handgrip test; (4) cold pressor test; and (5) heart rate response to deep breathing. Statistical analysis was performed using the Mann Whitney rank sum test; results of the test were considered significant at the 0.05 level. After tilting heart rate was significantly higher in CFS patients compared with healthy controls (mean CFS = 88.9 beats/min vs control = 77.9 beats/min; P <0.01).

Low frequency power after tilting was significantly higher in CFS patients compared with controls (mean CFS = 0.603 vs control = 0.428; P = 0.02). There was a trend toward an increased heart rate during the cold pressor test. Other parameters did not differ between the CFS and control populations.

The observed changes point toward a sympathetic overactivity in CFS patients when they are exposed to stress. Parasympathetic abnormalities could not be observed. Therefore, our findings provide no real explanation for the fatigue and intolerance to physical exertion in these patients.

 

Source: De Becker P, Dendale P, De Meirleir K, Campine I, Vandenborne K, Hagers Y. Autonomic testing in patients with chronic fatigue syndrome. Am J Med. 1998 Sep 28;105(3A):22S-26S. http://www.ncbi.nlm.nih.gov/pubmed/9790478

 

Neurally mediated hypotension and chronic fatigue syndrome

Abstract:

 

A substantial body of clinical evidence now supports an association between various forms of hypotension and both idiopathic chronic fatigue and the chronic fatigue syndrome (CFS). Patients with CFS have a high prevalence of neurally mediated hypotension, and open treatment of this autonomic dysfunction has been associated with improvements in CFS symptoms. Randomized trials are now in progress to evaluate the efficacy of treatments directed at neurally mediated hypotension in those with CFS patients, and the results of these trials should help guide more basic inquiries into the mechanisms of orthostatic intolerance in affected individuals.

 

Source: Rowe PC, Calkins H. Neurally mediated hypotension and chronic fatigue syndrome. Am J Med. 1998 Sep 28;105(3A):15S-21S. http://www.ncbi.nlm.nih.gov/pubmed/9790477

 

No strong evidence of disturbed regulation of blood pressure in chronic fatigue syndrome

Abstract:

Recent medical publications postulate a connection between the Chronic Fatigue Syndrome (CFS) and disturbed regulation of the circulation, manifesting itself during orthostatic stress testing.

Four studies were published on the circulatory response on prolonged head up tilt testing. Numerous CFS patients displayed postural tachycardia or syncope during the test. However, many CFS patients examined had had orthostatic symptoms prior to the examination.

It is not certain that cardiovascular dysregulation is present in CFS patients without orthostatic symptoms. It is also not clear whether such a dysregulation would be the effect of physical inactivity or a manifestation of a subtle form of autonomic neuropathy.

 

Source: Smit AA, Bolweg NM, Lenders JW, Wieling W. No strong evidence of disturbed regulation of blood pressure in chronic fatigue syndrome. Ned Tijdschr Geneeskd. 1998 Mar 21;142(12):625-8.[Article in Dutch] http://www.ncbi.nlm.nih.gov/pubmed/9623125

 

The role of delayed orthostatic hypotension in the pathogenesis of chronic fatigue

Abstract:

Past studies have shown that severe fatigue was the presenting symptom in six of seven patients with delayed orthostatic hypotension and that tilt table-induced hypotension was found in 22 of 23 patients with the chronic fatigue syndrome. We have determined the prevalence of fatigue, volunteered in response to a nonspecific pre-examination questionnaire used in 431 patients, each subsequently diagnosed as having one of eight neurological or endocrine disorders.

The results show that fatigue is a very common symptom in patients with delayed orthostatic hypotension (n = 21), as well as both primary (n = 30) and secondary (n = 106) hypocortisolism: 70-83% in all groups. In contrast, fatigue was an uncommon complaint in patients with multiple system atrophy (MSA) (n = 30), pituitary disorders without hypocortisolism (n = 106) or idiopathic hirsutism (n = 96): 7-33% in all groups, and was intermediate in prevalence in patients with acute hyperadrenergic orthostatic hypotension (n = 32): 41%.

It is concluded that fatigue commonly results from delayed orthostatic hypotension and all forms of hypocortisolism but is less common in patients with acute orthostatic hypotension, both idiopathic and due to MSA, which more commonly present with lightheadedness or syncope.

 

Source: Streeten DH, Anderson GH Jr. The role of delayed orthostatic hypotension in the pathogenesis of chronic fatigue. Clin Auton Res. 1998 Apr;8(2):119-24. http://www.ncbi.nlm.nih.gov/pubmed/9613802

 

Impaired associative learning in chronic fatigue syndrome

Abstract:

Patients with chronic fatigue syndrome (CFS) report cognitive difficulties (impaired attention, memory and reasoning). Neuropsychological tests have failed to consistently find cognitive impairments to the degree reported by CFS patients.

We tested patients with CFS and sedentary controls in protocols designed to measure sensory reactivity and acquisition of the classically conditioned eyeblink response. Patients with CFS exhibited normal sensitivity and responsivity to acoustic stimuli.

However, CFS patients displayed impaired acquisition of the eyeblink response using a delayed-type conditioning paradigm. Sensitivity and responsivity to the airpuff stimulus were normal.

In the absence of sensory/motor abnormalities, impaired acquisition of the classically conditioned eyeblink response indicates an associative deficit. These data suggest organic brain dysfunction within a defined neural substrate in CFS patients.

 

Source: Servatius RJ, Tapp WN, Bergen MT, Pollet CA, Drastal SD, Tiersky LA, Desai P, Natelson BH. Impaired associative learning in chronic fatigue syndrome. Neuroreport. 1998 Apr 20;9(6):1153-7. http://www.ncbi.nlm.nih.gov/pubmed/9601685

 

The connection between chronic fatigue syndrome and neurally mediated hypotension

Abstract:

Research from several groups of investigators indicates that some patients with chronic fatigue syndrome have abnormal vasovagal or vasodepressor responses to upright posture. If confirmed, these findings may explain some of the symptoms of chronic fatigue syndrome. There is also speculation that neurally mediated hypotension may be present in fibromyalgia. This article discusses the original research in this area, the results of follow-up studies, and the current approach to treating patients with chronic fatigue syndrome in whom neurally mediated hypotension is suspected.

 

Source: Wilke WS, Fouad-Tarazi FM, Cash JM, Calabrese LH. The connection between chronic fatigue syndrome and neurally mediated hypotension. Cleve Clin J Med. 1998 May;65(5):261-6. http://www.ncbi.nlm.nih.gov/pubmed/9599909

 

Alteration of spatial-temporal parameters of gait in Chronic Fatigue Syndrome patients

Abstract:

Chronic Fatigue Syndrome (CFS) has been widely studied and a lot of information is available in the literature regarding the immunological, virological, neuroendocrinal and psychiatric aspects of the disease, but its aetiology is still poorly understood. Great attention has also been paid to the alteration of the muscular function caused by CFS.

The aim of the present work was to study CFS patients’ gait in order to find out objective measures which can better characterize the pathology. Spatial and temporal parameters of gait were collected from a group of 12 CFS informed volunteers by using the typical instrumentation of movement analysis, and raw data were statistically elaborated.

Comparisons with reference data from a population of healthy subjects revealed significant abnormalities in the symmetry indices of the bilateral parameters and in the linear relationships among parameters, and between these parameters and the physical characteristics of the patients.

Interestingly, the abnormalities were present as from the beginning of the gait, which indicates that they are unlikely to be caused by the rapid increasing fatigue. This strengthens the hypothesis of a direct involvement of the central nervous system (CNS) in the onset of the disease.

 

Source: Saggini R, Pizzigallo E, Vecchiet J, Macellari V, Giacomozzi C. Alteration of spatial-temporal parameters of gait in Chronic Fatigue Syndrome patients. J Neurol Sci. 1998 Jan 21;154(1):18-25. http://www.ncbi.nlm.nih.gov/pubmed/9543318

 

Long- and short-term blood pressure and RR-interval variability and psychosomatic distress in chronic fatigue syndrome

Abstract:

1. Chronic low blood pressure has been associated with fatigue and low mood. However, in the chronic fatigue syndrome (CFS) the blood pressure (BP) and heart rate profile and their variabilities have not been characterized as yet.

2. We performed office and 24 h ambulatory BP recordings in 38 subjects (age, 34.8 +/- 8.0 years) who fulfilled the Holmes criteria for CFS and in 38 healthy control subjects (age 35.6 +/- 10.5 years), as well as short-term beat-to-beat BP and RR-interval recordings for 10 min in supine and standing position, and calculated spectral indices.

3. In CFS office (123 +/- 19/70 +/- 12 mmHg) as well as 24-h, day- and night-time blood pressure values (116 +/- 11.1/71 +/- 11.1, 121 +/- 9.2/77 +/- 8.0 and 110 +/- 10.5/65 +/- 9.2 mmHg respectively) were within reference limits.

4. Heart rate was consistently higher (P < 0.01) in CFS patients, based on both office (77 +/- 12 compared with 68 +/- 12 beats min-1) and 24 h ambulatory recordings (77 +/- 12 compared with 67 +/- 15 beats min-1).

5. In supine position, spectral indices of BP variability (total, low-frequency and high-frequency variances) were all significantly (P < 0.01) lower in CFS. In standing position the differences disappeared. Analysis of RR-interval variability could not detect major alterations in autonomic function in CFS.

Comment in: Long- and short-term blood pressure and RR-interval variability and psychosomatic distress in chronic fatigue syndrome. [Clin Sci (Lond). 1999]

 

Source: Duprez DA, De Buyzere ML, Drieghe B, Vanhaverbeke F, Taes Y, Michielsen W, Clement DL. Long- and short-term blood pressure and RR-interval variability and psychosomatic distress in chronic fatigue syndrome. Clin Sci (Lond). 1998 Jan;94(1):57-63. http://www.ncbi.nlm.nih.gov/pubmed/9505867

 

An investigation of sympathetic hypersensitivity in chronic fatigue syndrome

Abstract:

BACKGROUND: There are many theories, but the etiology of chronic fatigue syndrome (CFS) remains unknown. Diagnosticians have set guidelines to try to classify the condition, but its clinical definition is one of exclusion rather than defined by specific clinical testing. The primary goal of this investigation was to find a diagnostic key to define CFS. CFS patients and those diagnosed with the sympathetic hypersensitivity condition called fibromyalgia syndrome (FMS) exhibit identical brain single photon emission computerized tomography (SPECT) images. Therefore, this investigation was initiated to see if CFS patients also had denervation hypersensitivity of the sympathetic system.

METHODS: A standardized supersensitivity test was performed using an ocular instillation of two drops of 1.0% phenylephrine. Sixty-two subjects (29 CFS patients and 33 normals) participated in the study. Measurements of pupil size were recorded by pupil gauge and flash photography. A pupillary dilation of greater than 2.5 mm would suggest a sympathetic denervation hypersensitivity.

RESULTS: For all participants, a small, but statistically significant increase in pupil size was found (mean of 0.788 mm in normals and 0.931 mm in CFS patients). The change in pupil size in the CFS patients and controls showed substantial overlap and was not statistically significant (t = 0.83, p = 0.42, dF = 60).

CONCLUSION: In conclusion, the results suggest that a denervation hypersensitivity of the pupil does not occur in CFS patients. The use of 1.0% topical phenylephrine had no diagnostic value in detecting CSF patients vs. normals.

 

Source: Sendrowski DP, Buker EA, Gee SS. An investigation of sympathetic hypersensitivity in chronic fatigue syndrome. Optom Vis Sci. 1997 Aug;74(8):660-3. http://www.ncbi.nlm.nih.gov/pubmed/9323737