Posterior fossa syndrome with a large inflammatory ponto-mesencephalic lesion.

Demonstration of a posterior fossa syndrome (PFS) in a 32-year-old male patient with clinically isolated syndrome which subsequently developed into relapsing-remitting Multiple Sclerosis. The patient suffered from double vision, coordination problems including unsteady gait and atactic dysarthria, concentration difficulties, as well as adynamia and impaired decision making. The patient clinically presented a cerebellar and dysexecutive syndrome. Cerebral magnetic resonance imaging (MRI) revealed a contrast enhancing ponto-mesencephalic lesion with a volume of 4.8cm3. Neuropsychological tests showed pronounced executive dysfunctions, reduced visuoconstructive skills, attentional deficits, echolalia, and non-fluent speech production. After cortisone and plasmapheresis, the cerebellar syndrome improved but manual fine motor skills and executive dysfunctions persisted. After three months, symptoms remitted except for a slight gait imbalance. After six months, neuropsychological tests were normal except for a moderate attention deficit. MRI revealed a clear regression of the ponto-mesencephalic lesion to a volume of 2.4cm3 without contrast enhancement. This case report intends to provide an overview of the symptomatology and etiology of PFS and offers new insights into its pathomechanism demonstrating a pontine disconnection syndrome caused by a large demyelinating plaque.

Inherited cavernous malformations of the central nervous system: clinical and genetic features in 19 Swiss families.

Cavernous malformations (CCMs) are benign, well-circumscribed, and mulberry-like vascular malformations that may be found in the central nervous system in up to 0.5% of the population. Cavernous malformations can be sporadic or inherited. The common symptoms are epilepsy, hemorrhages, focal neurological deficits, and headaches. However, CCMs are often asymptomatic. The familiar form is associated with three gene loci, namely 7q21-q22 (CCM1), 7p13-p15 (CCM2), and 3q25.2-q27 (CCM3) and is inherited as an autosomal dominant trait with incomplete penetrance. The CCM genes are identified as Krit 1 (CCM1), MGC4607 (CCM2), and PDCD10 (CCM3). Here, we present the clinical and genetic features of CCMs in 19 Swiss families. Furthermore, surgical aspects in such families are also discussed.

Subcutaneous immunoglobulin: opportunities and outlook.

Immunoglobulin (Ig) administration via the subcutaneous (s.c.) route has become increasingly popular in recent years. The method does not require venous access, is associated with few systemic side effects and has been reported to improve patients' quality of life. One current limitation to its use is the large volumes which need to be administered. Due to the inability of tissue to accept such large volumes, frequent administration at multiple sites is necessary. Most studies conducted to date have investigated the use of subcutaneous immunoglobulin (SCIg) in patients treated previously with the intravenous (i.v.) formulation. New data now support the use of s.c. administration in previously untreated patients with primary immunodeficiencies. SCIg treatment may further be beneficial in the treatment of autoimmune neurological conditions, such as multi-focal motor neuropathy; however, controlled trials directly comparing the s.c. and i.v. routes are still to be performed for this indication. New developments may further improve and facilitate the s.c. administration route. For example, hyaluronidase-facilitated administration increases the bioavailability of SCIg, and may allow for the administration of larger volumes at a single site. Alternatively, more concentrated formulations may reduce the volume required for administration, and a rapid-push technique may allow for shorter administration times. As these developments translate into clinical practice, more physicians and patients may choose the s.c. administration route in the future.

MRI-based brain volumetry in chronic whiplash patients: no evidence for traumatic brain injury.

INTRODUCTION: Cognitive complaints, such as poor concentration and memory deficits, are frequent after whiplash injury and play an important role in disability. The origin of these complaints is discussed controversially. Some authors postulate brain lesions as a consequence of whiplash injuries. Potential diffuse axonal injury (DAI) with subsequent atrophy of the brain and ventricular expansion is of particular interest as focal brain lesions have not been documented so far in whiplash injury. OBJECTIVE: To investigate whether traumatic brain injury can be identified using a magnetic resonance (MR)-based quantitative analysis of normalized ventricle-brain ratios (VBR) in chronic whiplash patients with subjective cognitive impairment that cannot be objectively confirmed by neuropsychological testing. MATERIALS AND METHODS: MR examination was performed in 21 patients with whiplash injury and symptom persistence for 9 months on average and in 18 matched healthy controls. Conventional MR imaging (MRI) was used to assess the volumes of grey and white matter and of ventricles. The normalized VBR was calculated. RESULTS: The values of normalized VBR did not differ in whiplash patients when compared with that in healthy controls (F = 0.216, P = 0.645). CONCLUSIONS: This study does not support loss of brain tissue following whiplash injury as measured by VBR. On this basis, traumatic brain injury with subsequent DAI does not seem to be the underlying mechanism for persistent concentration and memory deficits that are subjectively reported but not objectively verifiable as neuropsychological deficits.

Evaluation of back pain secondary to spinal epidural hematoma associated with aspirin intake and a partial platelet glycoprotein Ia/IIa deficiency.

We report a case of spontaneous spinal epidural hemorrhage with three unusual features: (1) the hemorrhage was associated with aspirin ingestion and a reduced level of platelet glycoprotein Ia/IIa; (2) the patient presented with typical severe back pain but without neurologic dysfunction; and (3) the patient initially recovered without surgical decompression but suffered from recurrent epidural hematoma.

Neuralgia of the glossopharyngeal nerve in a patient with posttonsillectomy scarring: recovery after local infiltration of procaine-case report and pathophysiologic discussion.

We describe a patient with a three-year history of severe progressive left-sided glossopharyngeal neuralgia (GPN) that failed to adequately respond to various drug therapies. The application of lidocaine spray to the posterior pharyngeal wall provided no more than short-term relief. Apart from a large hypertrophic tonsillectomy scar on the left side all clinical and radiologic findings were normal. In terms of therapeutic local anaesthesia, the hypertrophic tonsillectomy scar tissue was completely infiltrated with the local anaesthetic (LA) procaine 1%. The patient has been almost completely pain-free ever since, and the lidocaine spray is no longer needed. Six weeks after the first treatment a repeat infiltration of the tonsillectomy scar led to the complete resolution of all symptoms. The patient has become totally symptom-free without the need to take any medication now for two and a half years. This is the first report of a successful therapeutic infiltration of a tonsillectomy scar using an LA in a patient with GPN that has been refractory to medical treatment for several years. A possible explanation may be that the positive feedback loop maintaining neurogenic inflammation is disrupted and "sympathetically maintained pain" resolved by LA infiltration.

Grey matter volumetric changes related to recovery from hand paresis after cortical sensorimotor stroke.

Preclinical studies using animal models have shown that grey matter plasticity in both perilesional and distant neural networks contributes to behavioural recovery of sensorimotor functions after ischaemic cortical stroke. Whether such morphological changes can be detected after human cortical stroke is not yet known, but this would be essential to better understand post-stroke brain architecture and its impact on recovery. Using serial behavioural and high-resolution magnetic resonance imaging (MRI) measurements, we tracked recovery of dexterous hand function in 28 patients with ischaemic stroke involving the primary sensorimotor cortices. We were able to classify three recovery subgroups (fast, slow, and poor) using response feature analysis of individual recovery curves. To detect areas with significant longitudinal grey matter volume (GMV) change, we performed tensor-based morphometry of MRI data acquired in the subacute phase, i.e. after the stage compromised by acute oedema and inflammation. We found significant GMV expansion in the perilesional premotor cortex, ipsilesional mediodorsal thalamus, and caudate nucleus, and GMV contraction in the contralesional cerebellum. According to an interaction model, patients with fast recovery had more perilesional than subcortical expansion, whereas the contrary was true for patients with impaired recovery. Also, there were significant voxel-wise correlations between motor performance and ipsilesional GMV contraction in the posterior parietal lobes and expansion in dorsolateral prefrontal cortex. In sum, perilesional GMV expansion is associated with successful recovery after cortical stroke, possibly reflecting the restructuring of local cortical networks. Distant changes within the prefrontal-striato-thalamic network are related to impaired recovery, probably indicating higher demands on cognitive control of motor behaviour.

Long-term outcome after whiplash injury. A 2-year follow-up considering features of injury mechanism and somatic, radiologic, and psychosocial findings.

With the increased incidence of whiplash injury following the introduction of compulsory car seat belts, a large number of reports have dealt with the aftermath of this condition. Previous studies, however, focused on somatic symptoms on the one hand or considered only psychological or neuropsychological variables on the other hand, often in loosely defined or selected groups of patients. No study so far has analyzed the long-term outcome in a nonselected group of patients using a clear injury definition considering patient history; somatic, radiologic, and neuropsychological findings; and features of the injury mechanisms assessed soon after trauma and during follow-up. the present investigation was designed to assess these combined factors. According to a strict definition of whiplash injury, we assessed a consecutive nonselected sample of 117 patients with recent injury who had similar sociocultural and educational backgrounds. The patients had been in automobile crashes and were all equally covered by accident insurance according to the country-wide scheme. Initial examination was performed 7.2 +/- 4.2 days after trauma, and follow-up examinations 3, 6, 12, and 24 months later. At baseline, features of injury mechanism, subjective complaints, and different aspects of patient history were documented and cervical spine X rays performed. At all examinations patients underwent neurologic examination and cognitive and psychosocial factor assessment. At 2 years, patients were divided into symptomatic and asymptomatic groups and then compared with regard to the initial findings. In addition, symptomatic patients who were disabled at the 2-year follow-up examination and symptomatic patients not disabled (that is, they were able to work at the pretraumatic level) were compared regarding initial and 2-year findings. At 2 years, 18% of patients still had injury-related symptoms. With regard to baseline findings the following significant differences were found: Symptomatic patients were older, had higher incidence of rotated or inclined head position at the time of impact, had higher prevalence of pretraumatic headache, showed higher intensity of initial neck pain and headache, complained of a greater number of symptoms, had a higher incidence of symptoms of radicular deficit and higher average scores on a multiple symptom analysis, and displayed more degenerative signs (osteoarthrosis) on X ray. In addition, symptomatic patients scored higher with regard to impaired well-being and performed worse on tasks of attentional functioning and showed more concern with regard to long-term suffering and disability.(ABSTRACT TRUNCATED AT 400 WORDS)

Ultrasound findings in spontaneous carotid artery dissection. The value of duplex sonography.

Extracranial and transcranial Doppler and duplex sonographic findings in six patients with internal carotid artery dissection proven by angiography is reported. Extracranial Doppler analysis showed occlusion without a recordable signal from the internal carotid artery at any level or stenosis with accelerated flow in the high cervical segment. Transcranial Doppler findings demonstrated the hemodynamic consequences of the internal carotid artery occlusion or stenosis with collateral flow across the circle of Willis and also showed the dampened pulse wave of the middle cerebral artery ipsilateral to the dissection. In duplex sonography, the indirect signs indicating internal carotid artery dissection were a patent carotid bifurcation and proximal internal carotid artery segment but with no or only a short systolic flow signal. Atherosclerotic wall changes were absent, an important finding that suggests nonatherosclerotic stenosis or occlusion. Direct signs making the diagnosis likely were a tapering of the internal carotid artery lumen distal to the bulb, an irregular membrane crossing the vessel lumen, and the demonstration of a true lumen with flow and a false one without flow. While cerebral angiography is still considered the gold standard, ultrasound may become the primary modality for early diagnosis. Doppler and duplex examinations help to indicate angiography and are the methods of choice for follow-up investigations. They clearly demonstrate spontaneous recanalization with normalization of carotid circulation or, in case of persistent occlusion, improvement of collateral blood supply. Sequential examinations may prove helpful to determine the duration of anticoagulant treatment.

Transcranial Doppler sonographic findings in middle cerebral artery disease.

The transcranial Doppler sonographic findings of 61 patients with middle cerebral artery (MCA) disease were compared with those of 535 controls. According to computed tomographic, angiographic, and/or autopsy findings, the patients were classified as having MCA occlusive lesions in the central (sphenoidal) part or in peripheral branches or MCA stenosis. With MCA lesions, the MCA flow velocity (FV) was reduced. At the same time the anterior cerebral artery FV increased because of collateral flow over leptomeningeal anastomoses. Central MCA lesions showed less marked changes than did peripheral lesions. In MCA stenosis a steep rise of MCA FV appeared inside the stenotic segment. If there was a high-grade stenosis or occlusion of the internal carotid artery, a collateral circulation over the anterior part of the circle of Willis was seen in addition to the changes caused by the MCA disease. From these hemodynamic changes, transcranial Doppler sonographic diagnostic criteria for MCA occlusive and stenotic lesions were established.

Cognitive functioning after common whiplash. A controlled follow-up study.

A random sample of 98 patients with common whiplash was examined early after trauma (mean +/- SD, 7.3 +/- 3.9 days) and again 6 months later. Cognitive functioning was assessed in conjunction with complaints, pain intensity, well-being, subjective cognitive impairment, neuroticism, and medication. At 6 months, 67 patients had fully recovered (asymptomatic group), while 31 were still symptomatic (symptomatic group). Symptomatic patients who were older at baseline, had a greater variety of symptoms, higher neck pain intensity, and greater subjective cognitive impairment. At baseline, both groups scored poorly on tests requiring complex attentional processing. All neuropsychological functions improved to normal at 6 months in both groups. This improvement cannot be explained by a practice effect, as shown by the results of normal volunteers. The symptomatic group showed delayed recovery regarding complex attentional functioning, which may be related to adverse effects of medication.

Neurosyphilis mimicking Miller-Fisher syndrome: a case report and MRI findings.

A 36-year-old man presented with rapidly progressive unsteadiness of gait and diplopia. He had horizontal nystagmus, left sixth nerve palsy, severe ataxia, and areflexia. CSF protein content was 2.4 g/L. Despite a pleocytosis, Miller-Fisher syndrome was diagnosed. Two years later, reevaluation revealed active neurosyphilis in the freshly drawn and stored serum and CSF samples. Clinical findings were consistent with tabes dorsalis. MRI showed lesions confined to the posterior columns of the spinal cord.

Ultrasound findings in carotid artery dissection: analysis of 43 patients.

BACKGROUND AND PURPOSE: To analyze the value of ultrasound for early diagnosis and follow-up of internal carotid artery dissection. METHODS: The carotid arteries were evaluated in 43 consecutive patients using extracranial and transcranial pulsed-wave Doppler and duplex sonography. RESULTS: Ultrasound examination was performed, on average, 7.7 days after the first symptoms. The dissections subsequently were verified by MRI (16 patients), angiography (13 patients), or both (14 patients) on average 4.4 days later. The overall sensitivity of the combined examination was 95% (93% for extracranial Doppler, 86% for transcranial Doppler, and 79% for duplex sonography). All three methods detected occlusions or high-grade stenoses in 100% of patients and moderate- or low-grade stenoses in 80% (combined methods), 70% (extracranial Doppler), 40% (transcranial Doppler), and 20% (duplex) of the patients. The findings in 33 patients with an occlusion or high-grade stenosis according to neuroradiology were as follows: absent flow signal in the internal carotid artery (100%) and biphasic (stump) flow in its bulb (86%), high-resistance flow pattern of the ipsilateral common carotid artery (91%), signs of collateral flow across the circle of Willis (97%), and low flow in the middle cerebral artery (79%) on transcranial insonation. In seven patients, a moderate stenosis of the high cervical carotid segment was found because of a retromandibular high-velocity signal. In five of them this was the only abnormal finding. Duplex examination was helpful because it confirmed absent internal carotid artery flow or stump flow in the case of occlusion or high-grade stenosis (100%) and excluded an atherosclerotic origin by demonstrating a patent bulb (100%) and the absence of plaques (95%). Follow-up studies showed recanalization in 63% of patients, occurring at variable intervals. Occlusion persisted in 37%. CONCLUSIONS: Ultrasound performed within the first weeks can corroborate a clinically suspected carotid dissection in up to 95% of patients. Repetitive follow-up studies in most cases are sufficient to monitor evolution.

Transient cerebral circulatory arrest coincides with fainting in cough syncope.

During prolonged coughing, intrathoracic and intra-abdominal pressures are transmitted via the great veins to the intracranial compartment, causing transient elevated intracranial pressure. The resulting reduction of cerebral perfusion pressure may cause a critical impairment of cerebral blood flow (CBF). Obstructive airway disease seems to be a prerequisite to build up the intrathoracic and intracranial pressures to a degree sufficient to compromise CBF and cause cough syncope. Using transcranial Doppler sonography (TCD) monitoring of middle cerebral artery flow velocities, we studied three patients with cough syncope. During coughing, they showed a transient cerebral circulatory arrest, which coincided with loss of consciousness in the two patients who fainted during TCD monitoring. EEG showed slowing, heart rate increased, and systemic arterial BP in one patient was preserved during the syncope. Our findings support the hypothesis that a critical reduction of CBF causes cough syncope.

Determination of language dominance: Wada test confirms functional transcranial Doppler sonography.

OBJECTIVE: To determine the efficacy of the invasive Wada test in determining language dominance, and to validate the functional transcranial Doppler sonography (fTCD) examination in patients. BACKGROUND: Previous work shows that simultaneous bilateral fTDC may identify cognitive hemispheric dominance in healthy individuals. METHOD: fTDC and the Wada test were performed prospectively in 14 patients with various diseases (tumors, cerebrovascular events, head injury, intractable epilepsy). fTDC hemispheric dominance was determined based on the hemispheric blood flow velocity shift for language and visuospatial tasks. RESULTS: fTDC was performed easily in patients. One patient could not be examined by fTDC because of absent temporal bone window for ultrasonic transmission. Two Wada tests were inconclusive due to patient somnolence. One of these patients suffered from right frontal tumor and had aphasia remitted under steroids when examined. fTDC indicated a bilateral language dominance. In the remaining 11 patients the correlation between fTDC and Wada language lateralization indices was 0.75 (p = 0.008). If a post hoc cutoff score was taken for the fTDC language lateralization index, in eight patients, both fTDC and Wada testing determined the left hemisphere to be dominant for language; in the other three patients, language function was bilateral in both examinations. CONCLUSION: Although the current results are preliminary and require replication in a larger sample, fTDC seems to be able to assess hemispheric language dominance not only in healthy individuals, but also in patients. It might become an alternative noninvasive or complementary tool to the Wada test, particularly in patients in whom the Wada test is impractical or gives inconclusive results.

Presenting symptoms and signs after whiplash injury: the influence of accident mechanisms.

OBJECTIVE: To assess the relationship between accident mechanisms and initial findings after whiplash injury. DESIGN: Cohort study. SETTING: Outpatient department, Department of Neurology, University of Berne, Switzerland. PATIENTS: A population-based sample of 137 consecutive patients referred by primary care physicians. Fractures or dislocations of the cervical spine, head trauma, and preexisting neurologic disorders were exclusion criteria. MAIN OUTCOME MEASURES: Patients were interviewed and examined within 7.2 days (SD, 3.9 days) after trauma. Analyzed accident features were position in the car, use of seat belt, head restraint and its point of head contact, damage to seat, head position and state of preparedness at the moment of impact, and type of collision. Analyzed symptoms were intensity and onset delay of post-traumatic head and neck pain; pain in the shoulders, back, and anterior neck; symptoms of neurologic dysfunction according to presumed origin--cranial nerve or brainstem, radicular or myelopathic; and a score of multiple symptoms. Analyzed signs were neck muscle tenderness and restricted neck movement, and signs of cranial nerve, brainstem, or radicular dysfunction. RESULTS: Passenger position in the car, use of seat belt, and the presence of a head restraint showed no significant relationship with findings. Rotated or inclined head position at the moment of impact was associated with a higher frequency of multiple symptoms (p = 0.045 and 0.008) with more severe symptoms and signs of musculoligamental cervical strain (p = 0.048 and 0.038) and of neural, particularly radicular (p = 0.031 and 0.019), damage. Unprepared occupants had a higher frequency of multiple symptoms (p = 0.031) and more severe headache (p = 0.046). Rear-end collision was associated with a higher frequency of multiple symptoms (p = 0.006), especially of cranial nerve or brainstem dysfunction (p = 0.00003). CONCLUSION: Three features of accident mechanisms were associated with more severe symptoms: an unprepared occupant; rear-end collision, with or without subsequent frontal impact; and rotated or inclined head position at the moment of impact.

Carotid dissection with and without ischemic events: local symptoms and cerebral artery findings.

OBJECTIVE: To study whether spontaneous dissections of the cervical internal carotid artery dissection (ICAD) with and without ischemia of the brain or retina differ in the prevalence of vascular risk factors, local neurologic signs and symptoms, and stenoses and occlusions of the cerebral arteries. METHODS: The authors prospectively studied 181 consecutive patients with 200 ICAD. Diagnosis was based on ultrasonography and MRI or catheter angiography. Vascular risk factors, presenting local (headache, neck pain, Horner syndrome, pulsatile tinnitus, cranial nerve palsy on the side of the ICAD) and ischemic signs and symptoms, and ultrasonographic findings in the carotid and basal cerebral arteries were evaluated. RESULTS: ICAD with ischemic events (n = 145) had a higher prevalence of hypercholesterolemia (p < 0.05), >80% stenoses and occlusions of the ICA (p < 0.0001), and intracranial obstructions (p < 0.001). ICAD without ischemic events (n = 55) had a higher prevalence of Horner syndrome (p < 0.001), cranial nerve palsy (p < 0.01), and normal ICA findings (p < 0.0001). CONCLUSIONS: These data suggest that ICAD causing high-grade stenosis and occlusion are more likely to lead to intracranial obstructions and cerebral or retinal ischemic events. Conversely, ICAD without luminal narrowing cause more local signs and symptoms.

Prognosis after percutaneous closure of patent foramen ovale for paradoxical embolism.

The long-term risk and risk factors for recurrent embolism after percutaneous closure of patent foramen ovale (PFO) were investigated in 152 consecutive patients with presumed paradoxical embolism. During follow-up, the actuarial freedom from recurrent embolism was 95.1% at 1 year, and 90.6% at 2 and 6 years. A residual shunt after percutaneous PFO closure was a predictor for recurrence (RR 5.3; 95% CI 1.3 to 21.0; p = 0.02). Randomized trials comparing medical treatment with percutaneous PFO closure in the prevention of recurrent embolism are in progress.

Adverse effects of intravenous immunoglobulin therapy.

A growing body of literature documents that intravenous immunoglobulin prophylaxis and therapy is becoming applied to a steadily growing list of new indications. Some of these new indications have led to the use of intravenous immunoglobulin therapy in doctors offices, far from the hospital environment. Being stable products purified from blood or plasma donations, intravenous immunoglobulins must be considered as biological products in addition to their status as pharmaceutical products. This makes the study of adverse reactions reach beyond a mere drug safety surveillance programme into the realms of good manufacturing procedures guaranteeing not only intravenous tolerance but also sterility with regard to transfusion transmitted agents. The initially perceived adverse effects, stemming from complement activating aggregated immunoglobulin G, had the effect of slowing down widespread introduction of intravenous immunoglobulin therapy in the late 1970s. These adverse effects have now been eliminated with amendment of the appropriate manufacturing steps. However, new adverse effects, such as hyperviscosity, aseptic meningitis or renal insufficiency, have been observed which can be assigned to certain comnpounds of intravenous immunoglobulin, to administration regimens or to special patient characteristics. Adverse effects can be divided into 3 types: immediate adverse effects (those that occur during the infusion, e.g. anaphylactoid reactions); delayed adverse effects (those that occur hours to days after initiation of the infusion, e.g. renal, pulmonary, dermatological adverse effects, hyperviscosity, aseptic meningitis, arthritis, cerebral infarction, haemolysis and leucopenia) and; late adverse effects (e.g. transmission of infectious agents). We conclude from our analysis, that in general, intravenous immunoglobulin may be considered a well tolerated medical agent provided the indication for use is chosen carefully and use is monitored by a physician familiar with contraindications, risks, adverse effects and their appropriate management.

Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients.

First symptoms and initial clinical, ultrasonographic and neuroradiological findings ascertained a mean of 5.6 days (SD = 5.6 days), 7.7 days (7.0), and 11.2 days (8.0) after symptom onset were analysed in 44 patients who suffered a spontaneous internal carotid artery dissection (ICD) verified by magnetic resonance imaging, angiography, or both. Common symptoms signalling dissection were unilateral headache in 68%, transient ischaemic attack in 20%, and cerebral infarction in 9%. Severe pain preceded cerebral ischaemia by more than 3 days in 60% of those patients who eventually suffered a stroke. However, only 2 were admitted because of pain alone and 33 for evolving neurological deficits. During the first month, ipsilateral severe headache occurred in 89%, neck pain in 36%, ipsilateral cerebral ischaemia in 82%, ocular ischaemia in 16%, oculosympathetic palsy in 48%, and cranial nerve palsy in 5%. Recent "trivial" head or neck trauma was elicited in 41%. Doppler and duplex sonography confirmed the clinical suspicion of ICD in 91.5% and in 96% of those with a significant stenosis or occlusion. MRI demonstrated a thickened vessel wall in all 33 imaged carotid dissections and a mural haematoma in 30. None of the 32 patients who received anticoagulant treatment subsequently deteriorated. Monitoring anticoagulant treatment with ultrasonographic follow-up studies demonstrated recanalization in 70% and persistent occlusion in 30%. The results demonstrate that familiarity with the initial symptoms, especially headache, and performance of an ultrasonographic study without delay are the cornerstones of an early diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)