Orbital phlebography in idiopathic intracranial hypertension and chronic tension-type headache.

BACKGROUND: Pathologic signs in orbital phlebographies have been reported in various neurological diseases. PURPOSE: To study if pathologic signs in orbital phlebography may be markers of inflammation primarily affecting intracranial capillaries, which would cause intracranial hypertension. MATERIAL AND METHODS: Two groups with different intracranial cerebrospinal fluid pressures (Pcsf) were compared as to inflammatory markers in serum and pathologic signs in orbital phlebographies. Nine consecutive patients with idiopathic intracranial hypertension (IIH) with bilateral papilledema and eight consecutive patients with chronic tension-type headache (CTTH) were investigated prospectively with fibrinogen, orosomucoid, haptoglobin in serum, and invasive orbital phlebograms. The angiograms were evaluated by two skilled neuroradiologists, independent of each other and without knowledge of the diagnoses or aim of the study, as to the following pathologic signs: (i) narrowing of superior ophthalmic veins; (ii) caliber changes of intraorbital veins; (iii) collaterals of intraorbital veins; (iv) flow to cavernous sinus; and (v) asymmetric drainage of cavernous sinus. RESULTS: Mean body mass index was >30 kg/m(2) in both groups. Pcsf was >200 < 250 mm H2O in 50% of the CTTH and >350 mm H2O in all IIH patients. No difference in inflammatory markers in blood was found. The phlebographies of the IIH patients had more pathologic signs and were considered pathologic significantly more often than the ones of the CTTH patients (P < 0.001). CONCLUSION: The difference as to phlebographic pathologic signs between the IIH and the CTTH patients with different Pcsf supports the hypothesis that such phlebographic signs are markers of inflammation primarily affecting intracranial capillaries, which would disturb cerebrospinal fluid regulation causing intracranial hypertension.

The relationship between idiopathic intracranial hypertension and obesity.

OBJECTIVE: Idiopathic intracranial hypertension (IIH) is usually considered to result from deficient intracranial absorption of cerebrospinal fluid, but has also been suggested to be caused by decreased cranial venous flow because of increased intrathoracic pressure resulting from intra-abdominal obesity. To test this hypothesis, cerebrospinal fluid pressure (Pcsf), extracranial venous pressure (Pvf), intracranial venous pressure, and body mass index (BMI) were studied in patients with IIH with papilledema compared with patients with chronic tension-type headache (CTTH). DESIGN AND SUBJECTS: The Pcsf and the pressures in frontal veins without (Pvf) and with bilateral compression of the supraorbital branch of the frontal veins and the superficial facial veins (Pvfc), the latter considered to be about equal to Pvfc, were studied in 10 consecutive patients with IIH with papilledema. Ten consecutive CTTH patients were used for controls. Orbital phlebography was performed to confirm that the compression of facial veins other than the frontal veins resulted in adequate communication between the frontal vein used for the studies and the cavernous sinus. RESULTS: Cerebrospinal fluid pressure was between 200 and 250 mm water in 5 of the CTTH patients and above 350 mm water in all IIH patients. Body mass index was >25 in all CTTH patients and similar in the 2 groups. Cerebrospinal fluid pressure was similar to Pvfc in all 10 CTTH patients but significantly greater in 6 of the 10 IIH patients. Pvf was similar in the 2 groups and related to BMI. CONCLUSIONS: Chronic tension-type headache patients may be prone to have Pcsf > 200 mm water and BMI > 25. Papilledema because of intracranial hypertension occurred in the present study at Pcsf > 350 mm water. The findings of Pvfc and Pcsf being similar in all CTTH patients support the suggestion that the techniques used for measuring intracranial venous pressure are adequate. The findings of similar BMI in the CTTH and the IIH patients who differed significantly as to Pcsf refute the hypothesis that obesity precedes, and is the cause of, intracranial hypertension in IIH. The difference between Pcsf and Pvfc in 6 of the IIH patients also does not support such a hypothesis but may indicate that IIH is due to deficient intracranial cerebrospinal fluid absorption. Since a relationship between intracranial hypertension and obesity is established and obesity is not found to cause intracranial hypertension in IIH, intracranial hypertension may be suggested to be the primary cause of weight increase in IIH. Obesity, however, may secondarily increase the preexistent IIH.

Treatment of idiopathic intracranial hypotension: cervicothoracic and lumbar blood patch and peroral steroid treatment.

METHODS: Twelve consecutive patients with clinical symptoms and testing results compatible with a diagnosis of idiopathic intracranial hypotension (IIH), but no identifiable site of cerebrospinal fluid (CSF) leakage, were treated with a cervicothoracic or lumbar epidural "blood patch" (EBP) or orally administered steroids. RESULTS: Prompt and complete relief from headache persisting for at least 4 months was attained in 3 of 4 treatments with cervicothoracic EBP, 2 of 15 with lumbar EBP, and 4 of 8 with steroids. CONCLUSION: These results suggest that in patients who presumably suffer from IIH and yet have no identifiable site of CSF leakage, the presumed leakage more often occurs at the cervicothoracic level than the lumbar. In addition, our experience suggests that some IIH patients may be treated effectively with oral steroids and a trial of such therapy may be considered as an alternative to EBP.

Peripheral postganglionic sympathicoplegia mimicking cluster headache attacks.

After dissection with complete occlusion of the internal carotid artery, a 58-year-old man started to suffer from intense cluster headache-like attacks. Magnetic imaging showed signs of nonsymptomatic cerebral emboli, which could be dated to have occurred in temporal relation to the start of the attacks, all on the right side. This case and two similar ones indicate that peripheral postganglionic sympathicoplegia can cause attacks with similar pain characteristics, accompanying symptoms, duration, and regularity as in cluster headache.

T Cell Ig- and mucin-domain-containing molecule-3 (TIM-3) and TIM-1 molecules are differentially expressed on human Th1 and Th2 cells and in cerebrospinal fluid-derived mononuclear cells in multiple sclerosis.

T cell Ig- and mucin-domain-containing molecules (TIMs) comprise a recently described family of molecules expressed on T cells. TIM-3 has been shown to be expressed on murine Th1 cell clones and has been implicated in the pathogenesis of Th1-driven experimental autoimmune encephalomyelitis. In contrast, association of TIM-1 polymorphisms to Th2-related airway hyperreactivity has been suggested in mice. The TIM molecules have not been investigated in human Th1- or Th2-mediated diseases. Using real-time (TaqMan) RT-PCR, we show that human Th1 lines expressed higher TIM-3 mRNA levels, while Th2 lines demonstrated a higher expression of TIM-1. Analysis of cerebrospinal fluid mononuclear cells obtained from patients with multiple sclerosis revealed significantly higher mRNA expression of TIM-1 compared with controls. Moreover, higher TIM-1 expression was associated with clinical remissions and low expression of IFN-gamma mRNA in cerebrospinal fluid mononuclear cells. In contrast, expression of TIM-3 correlated well with high expression of IFN-gamma and TNF-alpha. These data imply the differential expression of human TIM molecules by Th1 and Th2 cells and may suggest their differential involvement in different phases of a human autoimmune disease.

Blood pool scintigraphy of the skull in relation to head-down tilt provocation in patients with chronic tension-type headache and controls.

OBJECTIVE: To investigate the mechanisms behind the increase of chronic tension-type headache during head-down tilt. BACKGROUND: The pathophysiology of chronic tension-type headache is unknown. DESIGN AND METHODS: Ten patients suffering from chronic tension-type headache and 10 age- and sex-matched controls were studied with respect to pain intensity and alterations in cranial blood volume using planar scintigraphy and radiolabeled autologous erythrocytes before, during, and after head-down tilt, a procedure known to increase chronic tension-type headache. RESULTS: Four of 8 patients with chronic tension-type headache studied had increased cerebrospinal fluid pressure. During head-down tilt, the pain increased significantly in the group with chronic tension-type headache (P <.001) while the procedure did not cause headache in the controls. Blood volume significantly increased extracranially and decreased intracranially in both groups during head-down tilt. The extracranial nasal blood volume was significantly related to the pain experienced by the patients with chronic tension-type headache before and during head-down tilt. CONCLUSIONS: Although the changes in blood volume and, presumably, the increase of intracranial pressure were similar in the patients with chronic tension-type headache and the controls, only the patients experienced pain and pain increase during head-down tilt. This indicates that the pre-head-down tilt conditions must be different in the 2 groups and should be related to increased cerebrospinal fluid pressure/intracranial venous pressure in patients with chronic tension-type headache compared with controls. A difference in central mechanisms may, however, also be of importance for the difference in headache provocation in the 2 groups during head-down tilt.

Relationship between chronic tension-type headache, cranial hemodynamics, and cerebrospinal pressure: study involving provocation with sumatriptan.

OBJECTIVE: To study the relationship between chronic tension-type headache, cranial hemodynamics, and cerebrospinal pressure. BACKGROUND: Cerebrospinal pressure has been found to be above 200 mm in about 50% of patients with chronic tension-type headache. METHODS: Heart rate, blood pressure, common carotid artery diameter and blood flow, and craniovascular resistance and pain at regular intervals before, during, and after head-down tilt-a procedure which increases cerebrospinal pressure, were recorded. After head-down tilt, subcutaneous injections of either placebo or 6 mg of sumatriptan were administered. Chronic tension-type headache intensity before and after withdrawal of 20 mL of cerebrospinal fluid was documented. Cerebrospinal pressure and chronic tension-type headache intensity were measured after subcutaneous injection of 6 mg of sumatriptan. RESULTS: Head-down tilt provoked an increase of headache compared with baseline. Common carotid artery blood flow decreased and craniovascular resistance increased after sumatriptan injection, but not after placebo injection. The pain decreased after head-down tilt and placebo injection, but not after sumatriptan injection. Chronic tension-type headache intensity decreased in all 4 patients studied after withdrawal of 20 mL of cerebrospinal fluid. Cerebrospinal pressure increased in 5 patients with chronic tension-type headache after subcutaneous injection of 6 mg of sumatriptan with slight or no increase of pain. CONCLUSION: The results indicated that cerebrospinal pressure or intracranial venous pressure (or both) are related to chronic tension-type headache.

Coping style and social support in men and women suffering from cluster headache or migraine.

OBJECTIVE: To investigate similarities and differences between patients with cluster headache and patients with migraine. BACKGROUND: Patients with migraine and patients with cluster headache are considered, by many clinical neurologists, to be different psychologically and socially. METHODS: Twenty-five age-matched pairs of men and 24 age-matched pairs of women with either migraine or episodic cluster headache (men aged 31 to 62 years; mean, 47 years; women aged 23 to 72 years; mean, 44 years) were compared with regard to coping profiles as reflected in two "coping wheels," one for the present situation and one for the future. In addition, availability of attachment and social interaction was assessed by means of the ISSI (Interview Schedule for Social Interaction). RESULTS: Women with cluster headache anticipated fewer activities for themselves than women with migraine, and findings were similar in the male pairs. The men with cluster headache also anticipated significantly fewer activities for themselves in the present and with others in the present and in the future than the men with migraine. There was no significant difference as to emotional loading between the two groups. A tendency to more optimistic anticipation was found in the women with cluster headache. There were highly significant differences between the two groups in the "future" wheel. The group with migraine expected more concrete activities and more activities with their families in the future, and they also described their present situation to involve more activities with others. CONCLUSIONS: Results from the present study differ from those from studies utilizing more conventional questionnaires. In particular, we found that patients with cluster headache have fewer close social contacts than patients with migraine.

Right-lateralised central processing for pain of nitroglycerin-induced cluster headache.

Recent functional brain imaging studies with positron emission tomography (PET) suggest a preference of the right hemisphere, especially the anterior cingulate cortex (ACC), in affective processing of the clinical pain syndromes. We have investigated the central processing of cluster headache (CH) attacks provoked by sublingual nitroglycerin (NTG). In the cerebrum, provoked CH activated the ACC and the temporopolar region of the right hemisphere in addition to other regions. The regions activated in the ACC (Brodmann area (BA) 24 and 32) are involved in affective/cognitive processing of pain and willed attention. Our study discloses the preferential role of the right hemisphere in attributing emotional valence and attention to the suffering of pain. The findings support the theory of a right hemispheric specialisation in the mediation of withdrawal-related negative affect. The divergence of the distributed central processing between provoked cluster headache attack and experimentally induced acute pain indicates different central mechanisms for different types of pain.