This study has demonstrated that the most important variable in determining a successful treatment of chronic low back pain is the reduction of subjective feelings of disability in patients.
A series of 19 patients with what originally had been diagnosed as a first division (V1) trigeminal neuralgia was collected. The inclusion criteria were severe, rather short-lasting pain attacks within the V1 area, combined with trigger mechanisms. There were 10 women and 9 men, and the mean age of onset was 57.8 years. Fifteen of 16 with adequate information on attack duration had paroxysms of a "few seconds" duration or less, whereas 10 patients had paroxysms lasting < or = 2 seconds. In an exceptional case, only "more long-lasting" attacks (greater than 30 seconds' duration) were experienced. In regard to autonomic phenomena, lacrimation was most frequently present (in a total of 8 patients; 3 rather regularly, 5 more irregularly). The combination of lacrimation, conjunctival injection, and rhinorrhea was present in only 2 (of 19), and in neither of them in a major way. Typically, autonomic phenomena occurred during the later stages of disease and during particularly severe and long-lasting attacks. Seven of 14 with adequate information also had nocturnal attacks. Initially, a more or less complete carbamazepine effect was reported by 10 of 13 patients. Precipitation mechanisms were the same as with second and third division tic, but were mainly located within the V1 area, particularly initially. A comparison with SUNCT syndrome has been made. SUNCT is a predominantly male disorder, with only exceptional attacks of < or = 10 seconds' duration, and generally with attacks of 15 seconds or longer. Autonomic symptoms and signs are more pronounced than in V1 tic. Carbamazepine generally provides minor, if any, benefit in SUNCT. The present work strongly indicates that the two disorders are essentially different.
Sixteen patients suffering from hemicranial attacks are reported. After many years of unsuccessful conservative treatment (mean = 12.4 years), the patients were treated surgically with good results. The radiological or electrophysiological examinations were non-specific or negative. Only vasoactive tests (provoking or relieving pain) or local anesthesia proved helpful in diagnosing and localizing the origin of pain. Intraoperatively, hemicranial attacks were found to be caused by vascular irritation or compression of the cervical nerve root C2. After decompression (n = 6) or dissection (n = 10) of the nerve root and the ganglion, 12 patients were relieved of their pain, 2 had improved relatively, 1 showed only a slight improvement, and in 1 patient no cause was found and no improvement was achieved. Two patients suffered recurrence of pain postoperatively; one had no further complaints after root extirpation following percutaneous thermorhizotomy. Electron microscopic examination of the nerve root and its ganglion revealed focal morphological changes, including proliferation of connective tissue in the endoneurium and the ganglion itself, the formation of onion-bulb-like structures around single axons, discrete signs of myelin damage and axonal degeneration. These morphological changes are possibly the result of a chronic vascular compression.
We prospectively studied headache characteristics during 6 months after craniotomy performed for treatment of cerebral aneurysms in 79 patients. Semistructured interviews, headache diaries, the Hospital Anxiety and Depression Scale and the Epworth Sleepiness Scales, the Short Form-36 Health Survey (SF-36) and McGill Pain Questionnaire were used. Seventy-two patients had headaches, half before the fifth day after surgery. Changes were observed in headache diagnosis, side and site in the postoperative period. Headache frequency increased immediately after surgery and then decreased over time. Headache frequency was associated with depressive and anxiety symptoms. Pain intensity was higher in women and in patients with more anxiety symptoms. An incidence of post-craniotomy headache of 40% was observed according to International Headache Society classification criteria, 10.7% of the acute and 29.3% of the chronic type. The bodily pain domain of the SF-36 was worse in patients with more anxiety symptoms. Greater frequencies of headache were associated with lower scores on bodily pain and social functioning.
After many years of unsuccessful conservative treatment 16 patients suffering from hemicrania are relieved of their pain or are improved by operative treatment. Hemicranial attacks or permanent hemicrania is found to be caused by upper cervical nerve root compression. Vascular compression of C2 (n = 9) or scar tissue surrounding C2 (n = 1) or C3 (n = 1) is the pathology identified in cases of cervicogenic headache or "cluster headache-like" headache. Compression attributable to tumor, prolapsed disc, or spondylotic changes is found to be a cause of permanent headache. Only in those patients with permanent headache are radiological or electrophysiological findings helpful for diagnosis. In patients with hemicranial attacks and compression of nerve root C2 (n = 10) or C3 (n = 1), only vasoactive tests (provoking or relieving pain) or local anaesthesia prove to be helpful in diagnosing and localizing the origin of pain. The operation involves freeing the nerve roots from vascular compression. In two patients the C2 ganglion is resected. Thirteen patients subsequently become pain free. In three patients, hemicrania improves. Four of the 16 patients experience a recurrence of pain after the decompressive operation. After additional thermorhizotomy two patients have no further complaints and one patient has improved. One patient can tolerate his pain with occasional analgesics. The problem of referred pain into the fronto-ocular region is discussed.
Two male patients had a history of right-sided headache attacks occurring daily and spreading from the occipital to the frontal region. The attacks were accompanied by ciliary injections on the symptomatic side, increased lacrimation and, in one case, by rhinorrhea. The pain was relieved with vasoconstricting preparations (ergotamine) and provoked with vasodilating medications (nitroglycerine). A selective conduction anaesthesia of the C2 nerve root in one case and of the C2 and C3 roots in the other, temporarily relieved the pain. At operation, vessels were found which compressed these roots. Since decompression of the nerve roots, 3 years and 1 year ago respectively, the patients have remained free of pain.
For the time being, this operation should preferably be used in selected, chronic, severely afflicted, preferably elderly CEH patients, when other therapeutic approaches are exhausted.
We report a case of moyamoya disease (MMD) associated with arteriovenous malformation (AVM). The 30-year-old female patient presented with left-hemispheric transient ischaemic attacks (TIAs) involving dysphasia and right-sided hemiparesis. CT-scan and lumbar puncture showed no evidence of intracranial haemorrhage. Cerebral angiography revealed typical moyamoya vessels and occlusion of multiple cerebral arteries with consecutive collateral blood supply. Moreover, a left-parietal AVM with a diameter of approximately 2 cm was detected. An extra-intracranial arterial bypass (EIAB) connecting the left superficial temporal artery (STA) with a cortical branch of the left middle cerebral artery (MCA) was performed (STA-MCA anastomosis) and yielded subsequent resolution of the neurological deficit. Nine months post-operatively neurological deficits similar to those of the initial presentation recurred. Repeated angiography suggested comparatively increased AVM blood flow, and successful extirpation of the AVM gradually re-established almost full functional ability. However, deterioration of the neurological condition developed again. We herewith present the first European case of moyamoya disease associated with arteriovenous malformation and report the clinical course under an alternative neurosurgical treatment consisting of STA-MCA anastomosis and delayed extirpation of the AVM.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.