Cerebellar Ischemia Research Articles

Diagnosis of Vertebral Artery Dissection with Basiparallel Anatomical Scanning Magnetic Resonance Imaging

There is no consensus regarding the optimal method for diagnosing the dissection of intracranial arteries. We have developed a rapid and accurate examination method to diagnose vertebral artery dissection in the acute stage of cerebral infarction. Twenty-two patients with severe headache and neck pain and/or symptoms of brain stem or cerebellar ischemia underwent magnetic resonance imaging (MRI) with a 1.5-T scanner. Our protocol generated 3 contrast-weighted scans (T2-weighted, diffusion-weighted, and basi-parallel anatomical scanning [BPAS]-MRI) and conventional angiographs within 3 hours of the onset of symptoms. Then, we retrospectively analyzed the findings to identify the most reliable imaging method for diagnosing vertebral artery dissection in the acute stage of cerebral infarction. Based on the symptoms and the findings of T2-weighted imaging and conventional angiography, the initial diagnosis was dissection in 17 patients, lacunar infarction in 3 patients, and atherothrombosis in 2 patients. After follow-up studies the diagnosis was changed in 7 patients. The diagnosis based on symptoms and the findings of T2-weighted MRI and BPAS-MRI was dissection in 13 patients, atherothrombosis in 6 patients, and lacunar infarction in 3 patients. In 3 patients the diagnosis was changed during the follow-up phase. The diagnostic accuracy rate was higher with T2-weighted MRI and BPAS-MRI than with T2-weighted MRI and conventional angiography. We suggest that when intracranial vascular dissection is suspected, both the inner and outer contours of vessels must be inspected and that BPAS-MRI should be performed instead of conventional angiography to establish the definite diagnosis.

Ictal Downbeat Nystagmus in Cardiogenic Vertigo

Rotatory vertigo mostly develops in vestibular disorders while presyncopal dizziness usually reflects generalized cerebral ischemia due to a cardiovascular cause.1 Nevertheless, contrary to established wisdom, patients with cardiovascular disorders frequently report vertigo.1,–,3 However, the mechanism of so-called cardiogenic vertigo remains unknown. Furthermore, no study has explored vestibular dysfunction during a spontaneous episode in a patient with cardiogenic vertigo. The previous studies of induced syncope suggest that the vertigo may result from cerebellar ischemia and vestibular function was in fact assessed in one of these studies.4,5 We observed downbeat nystagmus during the presyncopal attack with vertigo in a patient with recurrent asystole due to sick sinus syndrome. ### Case report. A 67-year-old woman presented with recurrent rotatory vertigo, nausea, and palpitation for 3 months. The patient reported that the vertigo had lasted for 5–10 seconds, and occurred 2–3 times per week, which became more frequent for the previous several days. She had a history of mitral valve replacement 10 years before. Between the episodes, the …

Lateral Medullary Ischemia Presenting with Persistent Hiccups and Vertigo

ABSTRACTThis study describes a patient with lateral medullary ischemia (LMI) presenting with persistent hiccups followed by vertigo with horizontal head-shaking-induced contralesional nystagmus (HSN) and discusses pertinent pathophysiology. A 65-year-old man presented with persistent hiccups and disabling spells of vertigo, lasting 30 seconds that became much more frequent and associated with lateropulsion to the right. A strong left beating HSN was evident. Magnetic resonance imaging and angiography, and intra-arterial cerebral digital subtracted angiography showed subacute ischemic lesions in the right lateral medulla and ipsilateral inferior cerebellar hemisphere, and two tight stenoses of the V1 and V4 segments of the right vertebral artery. Patient was treated by intravenous heparin and oral clopidogrel. After 48 hours, hiccups disappeared. One month later, vertigo spells were less frequent but still disabling. Endovascular stenting of the right vertebral artery stenoses was then performed. In the subsequent four years, the patient had no further episodes of hiccups or vertigo. Less intense HSN persisted. Hiccups followed by vertigo, lateropulsion, and HSN had been the clinical presentation of LMI and cerebellar ischemia, without other major neurologic or ocular motor findings. This unusual clinical variant of LMI could mimic a more benign labyrinthine lesion, and possibly leading to a dangerously delayed treatment.

Young age and low temperature, but not female gender delay ATP loss and glutamate release, and protect Purkinje cells during simulated ischemia in cerebellar slices

Excessive activation of glutamate receptors contributes to Purkinje cell (PC) damage during brain ischemia, but the mechanisms of glutamate release are contentious. Age, gender and temperature all strongly influence ischemic brain damage, but the mechanisms underlying their influence are not fully understood. We determined how age, gender and temperature influence ATP loss, glutamate release, glutamate receptor activation and PC damage during cerebellar ischemia. We used voltage-clamped PCs to monitor glutamate release during simulated ischemia in slices of cerebellum of different ages and genders, and at different temperatures. While gender did not affect ischemic glutamate release, both young age and low temperature dramatically delayed the onset of glutamate release without affecting its magnitude. Glutamate receptor and transporter density were similar around young and old PCs, but the rate of ATP decline during ischemia was dramatically slowed in young animals and by lowered temperature. Bypassing the ischemia-induced loss of ATP, and disrupting ionic gradients directly by pharmacologically inhibiting the Na(+)/K(+)-ATPase, reduced the difference in timing of glutamate release in newborn and mature cerebellum. Ischemic damage in newborn and mature cerebellum paralleled ATP loss and glutamate release, but blocking glutamate receptors did not prevent ischemic damage. Thus, protection against brain ischemia provided by young age or lowered temperature is due to slower consumption and hence delayed loss of ATP, with a corresponding delay in glutamate release and other undetermined damage mechanisms. The protection afforded by female gender must occur downstream of ATP decline, glutamate release, and activation of glutamate receptors on PCs.

Video‐Assisted Removal of a Ventricular Mass through the Mitral Valve

We report the case of 31-year-old man who was admitted for cerebellar ischemia. The echocardiography showed an intraventricular mass, mobile with the cardiac activity compatible with a thrombus or a myxoma. He successfully underwent a video-assisted removal of the mass, through the mitral valve.

Lebensbedrohliche Differenzialdiagnosen des Drehschwindels und des Hörsturzes

Many patients call the ENT emergency department because of vertigo and sudden hearing loss. The majority of cases are due to peripheral or neurootological reasons. A serious and ongoing problem is that life-threatening ischemic, hemorrhagic and inflammatory diseases of the central nervous system may cause identical symptoms, making it difficult to differentiate between them. On the basis of our own patients with cerebellar ischemia, basilar thrombosis, dissection of the vertebral artery, cerebellar abscess, brain tumor and cholesteatoma and on the basis of expert opinions, typical sets of symptoms in patients with neurootological symptoms of a central cause are defined. To ensure early detection of these rare differential diagnoses, physicians should place particular importance on modern imaging diagnostics and neurological, interdisciplinary cooperation.

Downbeat nystagmus: aetiology and comorbidity in 117 patients

Objectives:Downbeat nystagmus (DBN) is the most common form of acquired involuntary ocular oscillation overriding fixation. According to previous studies, the cause of DBN is unsolved in up to 44% of...

Brain stem and cerebellar ischaemia complicating cervical zygapophysial joint neurotomy

A case report of the complication of postero-inferior cerebellar artery territory ischaemia in a 32-year-old woman during cervical zygapophysial joint neurotomy is presented. Possible causes and methods of avoiding this complication are discussed.

RESULTS OF MICROSURGICAL CLIPPING OF 50 HIGH COMPLEXITY BASILAR APEX ANEURYSMS

Complex basilar aneurysms (large size, wide base, low bifurcation, and dysmorphic posteriorly projecting domes) frequently fail endovascular treatment. We report our experience using the pretemporal transzygomatic transcavernous approach with 50 complex basilar aneurysms. Using the pretemporal transcavernous route, opening the occulomotor trigone, and removing the anterior clinoid and the posterior clinoid when necessary, a wide exposure of the interpeduncular fossa is achieved. Temporary clips are applied to a perforator-free zone of the basilar trunk, proximal to the superior cerebellar artery. Complexity criteria in the 50 aneurysms included large or giant size in 27 patients, wide dysmorphic base in 18 patients, low bifurcation in 21 patients, posteriorly projecting dome in 11 patients, and dolichoectasia of the apex in three patients. Twenty-five patients presented with subarachnoid hemorrhage. There were 14 men and 36 women between the ages of 32 and 76 years (mean, 52.2 yr). Forty-nine aneurysms (98%) were successfully clipped. There was no procedure-related mortality. Two patients died (one from delayed bowel ischemia and one from a vasospasm-related complication). There were three ischemia-related events, two of which were procedure-related (medial thalamic lacunar infarct, superior cerebellar distribution ischemia) and one which was a third distal middle cerebral cardiac embolus after stopping Coumadin (DuPont Pharmaceuticals, Wilmington, DE) for atrial fibrillation. Transient partial or complete occulomotor palsies occurred in all patients with full recovery as the rule, except in one patient. At discharge, Glascow Outcome Scale scores were 4 or 5 in 88% of the patients. At the 6-month follow-up examination, Rankin Outcome Scale scores were 0 to 2 in 92% of the patients. Our experience reintroduces microsurgery as a safe and more durable treatment option for the management of complex basilar apex aneurysms that tend to have a higher rate of failure with endovascular therapy.

Medial cerebellar stroke presenting as a pure labyrinthine syndrome

Objective: Cerebellar stroke may mimick vestibular neuritis, a benign and usually self-limited neurologic disorder. On the basis of the clinical findings it is not always possible to differentiate between those two entities. However, the differential diagnosis is important because treatment and surveillance of patients are different, and misjudging cerebellar infarction may be fatal as it may lead to swelling and brainstem compression. Recent studies and case reports on cerebellar ischaemia have shown that cerebellar infarction presenting as a pure labyrinthine syndrome, so-called pseudo-vestibular neuritis, is more common than previously thought.

Prospective Study of Positional Nystagmus in 100 Consecutive Patients

The purpose of this study was to investigate the various diagnoses of patients who present with positional nystagmus. Positional maneuvers were systematically performed in the plane of the posterior canal (PC; Dix-Hallpike maneuver) and the horizontal canal (HC; patients were rolled to either side in a supine position) on 490 consecutive patients essentially referred for vertigo and/or gait unsteadiness. One hundred patients (20%) presented positional nystagmus. This nystagmus had a peripheral origin in 83 patients, including 80 patients with benign paroxysmal positional vertigo (BPPV). In BPPV, the PC was involved in 61 patients, the HC in 18 patients (geotropic horizontal nystagmus in 11 and ageotropic in 7; changing from geotropic to ageotropic or the reverse in 4 patients), and both the PC and HC in 1 patient. There was evidence of central positional nystagmus in 12 patients, including positional downbeat nystagmus during the Dix-Hallpike maneuver in 7 patients with various neurologic disorders, and ageotropic horizontal nystagmus during the HC maneuver in 2 patients with, respectively, cerebellar ischemia and definite migrainous vertigo. The peripheral or central origin of the positional nystagmus could not be ascertained in 5 patients, including 1 patient with probable migrainous vertigo and another with possible anterior canal BPPV. A rotatory-upbeat nystagmus in the context of PC BPPV, a horizontal nystagmus, whether geotropic or ageotropic, due to HC BPPV, and a positional downbeat nystagmus related to various central disorders are the 3 most common types of positional nystagmus. Geotropic horizontal positional nystagmus and, most certainly, horizontal positional nystagmus changing from geotropic to ageotropic or the reverse point to HC BPPV. In contrast, an ageotropic horizontal positional nystagmus that is not changing (from ageotropic to geotropic) may indicate a central lesion.

The electrical response of cerebellar Purkinje neurons to simulated ischaemia

Despite lacking N-methyl-D-aspartate receptors, cerebellar Purkinje cells are highly vulnerable to ischaemic insults, which lead them to die necrotically in an -amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) receptor-dependent manner. To investigate the electrical events leading to this cell death, we whole-cell clamped Purkinje cells in cerebellar slices. Simulated ischaemia evoked an initial hyperpolarization of Purkinje cells by 8.5 mV, followed by a regenerative 'anoxic depolarization' (AD) to -14 mV. The AD was prevented by glutamate receptor blockers. In voltage-clamp mode, we used the cells' glutamate receptors to sense the rise of extracellular glutamate concentration induced by ischaemia, with GABA(A) and GABA(B) receptors blocked and Cs+ as the main pipette cation. Ischaemia induced a small (<500 pA) slowly developing inward current in Purkinje cells, followed by a sudden large inward 'AD current' (approximately 6 nA) which was largely prevented by blocking AMPA receptors. Removing extracellular calcium reduced the large glutamate-mediated current by approximately 70% at early times (after 10 min ischaemia), but had no effect at later times (15 min). Blocking the operation of glutamate transporters, by preloading cells with the slowly transported glutamate analogue PDC (L-trans-pyrrolidine-2,4-dicarboxylate), reduced the current by approximately 88% at early and 83% at later times. In Purkinje cells in slices from mice lacking the glial glutamate transporters GLAST or GLT-1, the ischaemia-evoked AD current was indistinguishable from that in wild-type slices. These data suggest that, in cerebellar ischaemia, the dominant cause of the electrophysiological dysfunction of Purkinje cells is an activation of Purkinje cell AMPA receptors. The glutamate activating these receptors is released both by exocytosis (at early times) and by reversal of a glutamate transporter, apparently in neurons.

Transcavernous approach to diseases of the anterior upper third of the posterior fossa

The region in the upper anterior third of the posterior fossa is a surgically hidden, narrow corridor between the petroclival surface anteriorly and the surface of the brainstem posteriorly. Although several approaches have been described to help surgeons reach this region, few of them enable practitioners to reach the different corners of the area and provide as wide a view as the one achieved using the transcavernous route. A transcavernous approach was used in 91 cases (50 complex upper basilar artery [BA] aneurysms, 30 upper petroclival junction meningiomas, five trigeminal nerve schwannomas, three upper clival chordomas, and three anterior pontine lesions) involving the anterior upper third of the posterior fossa. The approach uses the pretemporal route with exposure of the lateral wall of the cavernous sinus. It entails removal of the anterior clinoid process. The posterior clinoid process is also removed when necessary. The approach leads to the upper basilar region. It is widened inferiorly to expose the anterior aspect by removal of the posterior clinoid process and the petroclival osseous and dural elements. Its lateral extension exposes the region of the Meckel cave and it can be widened by removal of the petrous apex. Seventy patients experienced new transient mild cranial neuropathies, 67 of whom recovered fully. Surgically related ischemic morbidities occurred in three patients with BA aneurysms (one small medial thalamic infarct, ataxia due to superior cerebellar artery ischemia, and distal middle cerebral artery embolus in a patient with atrial fibrillation in whom anticoagulation therapy was stopped). All the neuropathies in patients with BA aneurysms were oculomotor and recovery was the rule in all of them. Three new permanent cranial neuropathies occurred in the patients with meningiomas. In seven patients with preoperative neuropathy, two had partial improvement. Five patients with atypical meningiomas were treated with postoperative radiation therapy. Progression occurred later in four patients who were treated with gamma knife surgery. There were no surgery-related deaths. More than 1 year of follow-up data were available in 85 patients, and 94% of those patients were in an active and functional state (Glasgow Outcome Scale scores of 4 and 5). The safety achieved with the transcavernous route allows surgeons to achieve wide exposures to lesions involving the anterior upper third of the posterior fossa. It is an approach that should be mastered by every neurosurgeon dealing with cranial lesions.

Neuroradiological features of vertigo.

The diagnostic pathway in a patient with vertigo starts with the accurate evaluation of medical history followed by a general physical and neurological examination. This step can often lead to the identification of the correct cause of the disease or, at least, to a distinction between peripheral and central vertigo. Neuroradiological investigations have to be considered as elective diagnostic procedures and include: computed tomography (CT), magnetic resonance (MR), MR angiography (MRA), angiography. For the diagnosis of peripheral vertigo, benign paroxysmal positional vertigo, labyrinthitis, Meniere disease, perilymphatic fistula, local trauma, toxic labyrinthitis, acute otitis media and chronic middle ear effusion,the role of imaging techniques is controversial. CT and MR are performed to rule out other pathologies and to confirm the diagnosis. Increased resolution and application of special MR sequences enhancing the intralabyrinthine fluids have enabled more detailed analysis of labyrinthine structures and pathology. Both T2 and T1 contrast sequences are necessary. A high resolution CT study is required when otitis media is suspected and in the follow-up of post-traumatic vertigo. The causes of central vertigo are numerous and include: vertebro-basilar circulation vascular events, multiple sclerosis (MS), migraine-associated vertigo, cerebellar and brainstem tumors, CNS infections. Among them cerebrovascular ischemia and multiple sclerosis are the most frequent. In these situations imaging studies become mandatory. CT can diagnose most cerebellar hemorrhages and some cerebellar and brainstem acute ischemia, enhanced MR has proved to be the most sensitive tool to detect posterior fossa lesion. Diffusion-weighted MR can reveal acute ischemic changes before routine MR. There has been evidence that MR angiography, providing angiogram-like images of the intracranial vessels may sometimes avoid invasive angiography. MRA resolution is not as good as traditional angiography and may also be compromised by movements and other artifacts. Selective angiography of the posterior circulation is often indicated for therapeutic decisions.

Vertigo secondary to isolated PICA insufficiency: successful treatment with balloon angioplasty

Background The posterior inferior cerebellar arteries (PICA) arise from the intracranial segments of the vertebral artery (VA). We report a case where a nondominant isolated vertebral artery, which terminated in PICA, was stenotic. This resulted in brainstem-lower cerebellar ischemia, corrected with balloon angioplasty. Case description A 62-year-old male presented primarily with transient vertigo, syncope, and dizziness and was diagnosed with transient ischemic attack. Angiography of the left vertebral artery (VA) demonstrated a small-caliber vessel terminating in PICA with a 90% stenosis at the C6 level. Angioplasty of the left VA was performed with excellent resolution of the stenosis. Conclusions This case illustrates cerebellar insufficiency in a unique case where the PICA was isolated, supplied by a small- caliber VA. Correction of the stenosis improved the patient's symptomatology and prevented an inferior brainstem-cerebellar infarction.

Cerebellar speech representation: lesion topography in dysarthria as derived from cerebellar ischemia and functional magnetic resonance imaging.

Lesion topography and the pathophysiological background of dysarthria due to focal cerebellar lesions have not yet been fully clarified. To investigate the lesion topography of dysarthria due to cerebellar ischemia and evaluate brainstem functions. Case studies. Eighteen right-handed patients with sudden-onset dysarthria and cerebellar ischemia with and without brainstem involvement and 19 healthy, right-handed, monolingual, German-speaking volunteers. In patients, we used multimodal electrophysiologic techniques to investigate brainstem functions. Functional magnetic resonance imaging (MRI) was performed in the 19 healthy volunteers. Activation tasks consisted of repetitive vertical silent movements of the tongue and lips at a self-paced rhythm. Cerebellar lesions and additional signs of brainstem involvement were observed in 11 patients with posterior inferior cerebellar artery, anterior inferior cerebellar artery, and superior cerebellar artery infarctions, respectively. In all other patients with isolated cerebellar infarction (n = 7), only the superior cerebellar artery territory (6 right-sided, 1 left-sided) was affected, and the common lesion site was the rostral paravermal region of the anterior lobe. Functional MRI in healthy volunteers indicated that the cerebellar representation of the tongue and orofacial muscles corresponds to that of the area involved in patients with cerebellar dysarthria. The results of this study demonstrate that articulatory movements of the tongue and orofacial muscles are involved in the activation of the rostral paravermal area of the anterior lobe. This location corresponds to the area involved in cerebellar ischemia in patients with dysarthria. Lesions in the upper paravermal area of the right cerebellar hemisphere, the site of coordination of articulatory movements of the tongue and orofacial muscles, may lead to the development of dysarthria that is unrelated to (often concomitant) brainstem infarctions.

Plasticity of motor representation within the cerebellum after cerebellar ischemia

Plasticity of motor representation within the cerebellum after cerebellar ischemia

Risk factors and precipitating neck movements causing vertebrobasilar artery dissection after cervical trauma and spinal manipulation.

Potential precipitating events and risk factors for vertebrobasilar artery dissection were reviewed in an analysis of the English language literature published before 1993. To assess the literature pertaining to precipitating neck movements and risk factors for vertebrobasilar artery dissection in an attempt to determine whether the incidence of these complications can be minimized. Vertebrobasilar artery dissection and occlusion leading to brain stem and cerebellar ischemia and infarction are rare but often devastating complications of cervical, manipulation and neck trauma. Although various investigators have suggested potential risk factors and precipitating events, the basis for these suggestions remains unclear. A detailed search of the literature using three computerized bibliographic databases was performed to identify English language articles from 1966 to 1993. Literature before 1966 was identified through a hand search of Index Medicus. References of articles obtained by database search were reviewed to identify additional relevant articles. Data presented in all articles meeting the inclusion criteria were summarized. The 367 case reports included in this study describe 160 cases of spontaneous onset, 115 cases of onset after spinal manipulation, 58 cases associated with trivial trauma, and 37 cases caused by major trauma (3 cases were classified in two categories). The nature of the precipitating trauma, neck movement, or type of manipulation that was performed was poorly defined in the literature, and it was not possible to identify a specific neck movement or trauma that would be considered the offending activity in the majority of cases. There were 208 (57%) men and 158 (43%) women (gender data not reported in one case) with an average age of 39.3 +/- 12.9 years. There was an overall prevalence of 13.4% hypertension, 6.5% migraines, 18% use of oral contraception (percent of female patients), and 4.9% smoking. In only isolated cases was specific vascular disease such as fibromuscular hyperplasia noted. The literature does not assist in the identification of the offending mechanical trauma, neck movement, or type of manipulation precipitating vertebrobasilar artery dissection or the identification of the patient at risk. Thus, given the current status of the literature, it is impossible to advise patients or physicians about how to avoid vertebrobasilar artery dissection when considering cervical manipulation or about specific sports or exercises that result in neck movement or trauma.

Phonemic Vowel Length Contrasts in Cerebellar Disorders

Apraxia of speech and Broca's aphasia both affect voice onset time (VOT) whereas phonemic vowel length distinctions seem to be preserved. Assuming a close cooperation of anterior perisylvian language zones and the cerebellum with respect to speech timing, a similar profile of segment durations must be expected in ataxic dysarthria. In order to test this hypothesis, patients with cerebellar atrophy or cerebellar ischemia were asked to produce sentence utterances including either one of the German lexial items “Rate” (/ra:the/, ‘installment’), “Ratte” (/rathe/, ‘rat’), “Gram” (/gra:m/, ‘grief’), “Gramm” (/gram/, ‘gramm’), “Taten” (/thatn/, ‘actions’), or “Daten” (/datn/, ‘data’). At the acoustic signal, the duration of the target vowels /a/ and /a:/ as well as the VOT of the word-initial alveolar stops /d/ and /t/ were determined. In addition, a master tape comprising the target words from patients and controls in randomized order was played to three listeners for perceptual evaluation. In accordance with a previous study, first, the cerebellar subjects presented with a reduced categorical separation of the VOT of voiced and unvoiced stop consonants. Second, vowel length distinctions were only compromised in case of the minimal pair “Gram”/“Gramm.” In contrast to “Rate”/“Ratte”, production of the former lexical items requires coordination of several orofacial structures. Disruption of vowel length contrasts would, thus, depend upon the complexity of the underlying articulatory pattern.

Diagnosis of Vertebrobasilar Insufficiency: Time to Rethink Established Dogma?

As isolated symptoms, vertigo, dizziness and imbalance are not regarded by neurologists as reflections of transient ischemia in the vertebrobasilar circulation. The purpose of this retrospective study was to demonstrate that these symptoms can and do occur in isolation. To this end, we analyzed the symptoms, stroke risk factors and diagnostic algorithms in 27 patients with a diagnosis of transient vertebrobasilar ischemia. None of the 27 patients included in the review complained of any associated neurologic symptoms. Against the reference standard of brain imaging, the site of the pathologic lesion was defined in the brainstem/cerebellum with the Torok monothermal caloric test, with a sensitivity greater than 86%. Vestibular decruitment and hyperactive caloric responses were of particular diagnostic value. Thus, we recommend that the neurologic dogma with regard to brainstem cerebellar ischemia be rethought.