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S Förderreuther

Publications and source records attributed to S Förderreuther.

At least 19 recordsLinked to original sources
PubMed2006

Opioidergic changes in the pineal gland and hypothalamus in cluster headache: a ligand PET study.

Using PET with the opioidergic ligand [11C]diprenorphine, the authors demonstrate decreased tracer binding in the pineal gland of cluster headache patients vs healthy volunteers. Opioid receptor availability in the hypothalamus and cingulate cortex depended on the duration of the headache disorder. Therefore, the pathophysiology of cluster headache may relate to opioidergic dysfunction in circuitries generating the biologic clock.

Adult↗
PubMed2006

[Motor cortical representation in patients with complex regional pain syndrome: a TMS study].

In a group of patients with short- and long-term (chronic) duration of complex regional pain syndrome type I (CRPS I) motor cortical representation was determined, using a transcranial magnetic stimulation (TMS) mapping method. This was done, starting with suprathreshold intensities at the location of the largest MEP amplitude, mapping systematically in all directions. Patients were compared to a group of healthy subjects. In both patient groups we found significantly larger motor cortical representation for the unaffected hand muscles compared to the affected side. This asymmetry was absent in healthy subjects. Such motor cortical representation asymmetry can be considered an effect of altered sensomotor cortical representation. On the other hand, one must also consider the increased use of the unaffected hand and the presence of pain as cortical influencing variables. The real cause must remain speculative at this time.

Adolescent↗
PubMed2006

Quantitative sensory testing in cluster headache: increased sensory thresholds.

To determine if recently reported changes in sensory thresholds during migraine attacks can also be seen in cluster headache (CH), we performed quantitative sensory testing (QST) in 10 healthy subjects and in 16 patients with CH. Eight of the patients had an episodic CH and the other eight a chronic CH. The tests were performed on the right and left cheeks and on the right and left side of the back of the hands to determine the subjects' perception and pain thresholds for thermal (use of a thermode) and mechanical (vibration, pressure pain thresholds, pin prick, von Frey hairs) stimuli. Six patients were examined in the attack-free period. Three were also willing to repeat the tests a second time during an acute headache attack, which was elicited with nitroglycerin. The healthy subjects performed the experiments in the morning and evening of the same day to determine if sensory thresholds are independent of the time of day. If they were, this would allow estimation of the influence of the endogenous cortisone concentration on these thresholds. The control group showed no influence of the time of day on the thresholds. There was a significant difference in pain sensitivity between the back of the hands and the cheeks (P<0.05): higher thresholds were found on the back of the hands. The thresholds generally exhibited little intersubject variability, indicating that QST is a reliable method. There was also a significant difference between the test areas in the patient group (P<0.001): the cheeks were also more sensitive than the back of the hands. In comparison with reference data of healthy volunteers, the detection thresholds were increased in the patients on both test areas. These were statistically significant for warmth, thermal sensory limen (TSL), heat and pressure on the back of the hands (P<0.04) and for the warmth and TSL thresholds on the cheeks (P<0.05). There were no differences in the thresholds regardless of whether the patients were examined in or outside of a cluster bout. Furthermore, we found no cutaneous allodynia in the three patients tested during an attack. The increased sensory thresholds on the cheeks as well as on the back of the hands are in agreement with an increased activation of the patients' antinociceptive system. The seasonal variation and the temporal regularity of single attacks as well as the findings in imaging studies indicate that the hypothalamus is involved in the pathophysiology of CH. In view of the strong connectivity between the hypothalamus and areas involved in the antinociceptive system in the brainstem, we hypothesize that this connection is the reason for the increased sensory thresholds in CH patients found in our study.

Adaptation, Physiological↗
PubMed2004

[Sleeping behaviour and headache attacks in cases of primary headache. Possible pathological mechanisms].

Headache is connected with sleep quality, e.g. hypnic headache and chronic paroxysmal headache attacks occur preferentially during REM sleep; this is possibly also true for cluster headache and migraine. REM sleep is typically characterized by the occurrence of ponto-geniculo-occipital spikes (PGOs). These PGOs should be able to trigger cortical spreading depression (CSD), which, although often clinically silent, is assumed to be an essential element of a migraine attack and possibly also of other forms of headache. CSDs are considered a correlate of migraine aura. They could lead to the secondary activation of trigeminovascular afferences, which would then induce a headache. Interestingly, illnesses that are comorbid with migraine cause an increase in the amount of REM sleep; conversely, various drugs administered prophylactically for these illnesses reduce the quantity of REM sleep.

Chronic Disease↗
PubMed2004

[Symptomatic headache. Essential differential diagnosis].

A patient is suspected of suffering from a potentially life threatening headache according to the following typical warning signs: sudden onset headache, worst headache, neurological findings, fever, neck stiffness, epileptic seizures and deterioration of vigilance. It is far more dangerous not to recognize potentially life threatening headaches like subarachnoid bleeding, meningitis, encephalitis, arterial dissection or epidural hematoma than to over diagnose it. Immediate and specific neurological and radiological investigations (CT, MRI, CSF) are necessary in each patient presenting with those findings. The morbidity and mortality of those patients mainly depend on the beginning of the therapy. This article focuses on the diagnosis of potentially life threatening headache disorders.

Diagnosis, Differential↗
PubMed2004

Impaired self-perception of the hand in complex regional pain syndrome (CRPS).

To investigate neglect, extinction, and body-perception in patients suffering from complex regional pain syndrome (CRPS). So-called 'neglect-like' symptoms have been reported in CRPS, however no studies have yet analyzed this phenomenon which might substantiate the theory of the central nervous system involvement in the pathophysiology of CRPS. A total of 114 patients with CRPS of the upper limb underwent bedside neurological examination. 'Neglect-like' symptoms were determined by asking all patients what kind of feeling they had toward the affected hand (feeling of foreignness). Hemispatial neglect was tested with the line bisection task in 29 patients and sensory extinction to simultaneous stimulation in 40 patients. The ability to identify fingers after tactile stimulation was tested in 73 patients. Independently of the affected side and disease duration, 54.4% of the patients reported that their hand felt 'foreign' or 'strange'. The ability to identify fingers was impaired in 48% on the affected hand and in 6.5% on the unaffected hand ( X(2) = 33.52, df = 1, p < 0.0001). These findings were related to pain intensity, illness duration and the extent of sensory deficits. No typical abnormalities indicating neglect were found in the line bisection test. Sensory extinction was normal in all patients. A large proportion of CRPS patients have disturbances of the self-perception of the hand, indicating an alteration of higher central nervous system processing. There are no indicators that classic neglect or extinction contribute to these findings. Physical therapy of such patients should take this observation into consideration.

Adolescent↗
PubMed2003

Decreased sTNF-RI in migraine patients?

Tumour necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) have recently been found to have a pain-mediating function in addition to their immunological, proinflammatory function. According to the hypothesis of neurovascular inflammation in migraine, these two cytokines could contribute to migraine pain generation. We analysed IL-6 and its soluble receptors sIL-6R and sgp130 as well as TNF-alpha and its soluble receptor sTNF-RI in 27 migraine patients and eight headache-free controls. Migraine patients tended to have less sTNF-RI (794 +/- 158 pg/ml) than controls (945 +/- 137 pg/ml). No differences in cytokine concentrations were observed. If TNF-alpha plays a role in migraine physiopathology, migraine patients may lack sufficient antagonistic sTNF-RI to neutralize hyperalgesic TNF-alpha during a migraine attack.

Adult↗
PubMed2003

Soluble interleukin-2 receptors increase during the active periods in cluster headache.

OBJECTIVE: To investigate whether cytokines are altered during the active period of cluster headache. BACKGROUND: Patients with cluster headache show activation of the hypothalamus in PET studies and via endocrinologic parameters. Data also suggest an inflammatory process occurs in cluster headache. A connection between the presumed inflammatory cause, an immunological activation, and the hypothalamus could be generated by certain cytokines. DESIGN AND METHODS: ELISA was used to determine the serum levels of soluble interleukin-2 receptors, interleukin-1, interleukin-6, and 2 soluble interleukin-6 receptors (sIL-6R and soluble gp130) in 18 patients with cluster headache (6 women and 12 men) during the cluster period and in 17 healthy controls who were headache-free (3 women and 14 men). RESULTS: Patients with cluster headache had significantly increased soluble interleukin-2 receptors (413.6+/-223 U/mL vs. 290.0+/-112 U/mL; P <.05) compared with controls. Serum levels of interleukin-1 (0.29+/-0.30 pg/mL vs. 0.13+/-0.13 pg/mL, n.s.), interleukin-6 (0.87+/-0.6 pg/mL vs. 0.91+/-0.7 pg/ml; n.s.), soluble interleukin-6 receptors (33,131+/-8,349 pg/mL vs. 35,063+/-7,606 pg/mL; n.s.), or soluble gp130 (289+/-59 pg/mL vs. 283+/-20 pg/mL; n.s.) did not differ between the 2 groups, although patients with cluster tended to have higher interleukin-1 values. CONCLUSIONS: Because elevated soluble interleukin-2 receptors indicate T cell activation, our findings suggest immune activation during cluster headache. Because interleukin-2 can activate the hypothalamus and stimulate the release of Corticotropin-releasing Factor (CRF), interleukin-2 could link a putative immunological cause of cluster headache with the observed hypothalamic activation. Systemic changes of interleukin-1 or the interleukin-6 system do not seem to play a role in cluster headache, as no alterations of serum levels were observed. Even so, unchanged serum levels do not exclude limited local production.

Adult↗
PubMed2002

Treatment of cluster headache with topiramate: effects and side-effects in five patients.

We report on clinical experience with topiramate in the prophylactic treatment of three patients with chronic and two patients with episodic, otherwise therapy-resistant, cluster headache. Patients were treated with daily doses of 75-200 mg topiramate. Topiramate was effective in three patients but proved ineffective and also caused intolerable side-effects in two patients. Topiramate may have prophylactic properties for treating cluster headache at lower doses than needed in epilepsy therapy, but its clinical value is limited due to central nervous system side-effects.

Adult↗
PubMed2001

Dilated cervical epidural veins and extra arachnoid fluid collection in orthostatic headaches.

Cervical MRI of eight patients with severe orthostatic headache showed a convex-shaped, prominent, dilated anterior, internal vertebral venous plexus with a flow-void signal in all patients and in seven also extra arachnoid fluid collection. Follow-up MRI showed resolution of the abnormalities in all patients. The authors hypothesize that these findings reflect disturbed compensatory vascular mechanisms by which autoregulation of the CSF pressure tries to compensate for the reduced CSF volume.

Adult↗
PubMed2001

[Important acute measures after fractures. Rapid and adequate treatment of pain].

Pain caused by bone fractures needs to be treated promptly and adequately to avoid negative secondary effects. Pain therapy and the healing of soft tissue are goals that are equally as important as healing of the fracture. The following factors have analgesic potential: reduction, immobilization, cooling measures, limb elevation and fasciotomy. Symptomatic treatment of pain is orientated to the WHO stepped approach, which attaches particular importance to the regular administration of analgesics, as dictated by clinical effectiveness.

Analgesics↗
PubMed2001

[When fracture pain does not subside. Recognizing complications].

Over the long term, the evolution of pain caused by fractures is determined by the quality of immobilization, the extent of edema, and by surgical, analgesic and physiotherapeutic treatment. Development of chronicity is initiated by secondary deterioration, persistence of pain in the absence of improvement, changes in the nature of the pain, its spontaneous occurrence, and the appearance of concomitant symptoms. Differential diagnostic considerations must include surgical complications, but also damage to nerves, or the complex regional pain syndrome (CRPS). A particular differential diagnostic problem is the differentiation between CRPS and other complications. Treatment must be matched to the diagnosis: conservative attempts at treatment may have to be followed up with surgical revision. Drug treatment of pain is oriented to the stepped WHO schema. Physiotherapy, physical treatment and ergotherapy play a major role in the treatment of CRPS.

Chronic Disease↗
PubMed2001

Cervical MR imaging in postural headache: MR signs and pathophysiological implications.

BACKGROUND AND PURPOSE: Postural headache most often occurs after lumbar puncture as post-lumbar puncture headache (PLPH) or, rarely, spontaneously as spontaneous intracranial hypotension headache (SIHH). In this prospective study, we used spinal MR imaging to determine the findings that would assist in the diagnosis of PLPH and SIHH and that would further our pathophysiological understanding of postural headache. METHODS: The study group consisted of 15 healthy volunteers and 20 patients with postural headache: nine with SIHH and 11 with PLPH. The craniocervical junction and the cervical spine were studied using T2-weighted fast spin-echo and T1-weighted spin-echo sequences in the axial and sagittal planes. Follow-up studies were performed in 13 patients. RESULTS: Dilatation of the anterior internal vertebral venous plexus was the most constant finding, present in 17 (85%) of 20 patients with postural headache. Spinal hygromas, whose location as subdural or epidural could not be exactly determined, were present in 14 patients (70%). A focal fluid collection was detected in the retrospinal region at the C1-C2 level in six patients with SIHH and in four patients with PLPH (50%). Tonsillar descent was detected in only one patient, and subtentorial hygroma in five patients. No abnormalities were found in the volunteers. CONCLUSION: The MR signs of dilatation of the venous plexus, presence of spinal hygromas, and presence of retrospinal fluid collections can help to establish the diagnosis of intracranial hypotension. They are probably the result of decreased CSF volume, with the retrospinal fluid collections being a transudate from the venous plexus rather than frank extravasation. Resolution of these signs parallels resolution of the headache.

Adult↗