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Benign paroxysmal positional vertigo (BPPV) is the most frequent form of vertigo seen in patients attending emergency departments. Leading symptoms are short attacks of vertigo provoked by head or body rotations. BPPV is caused by small calcium crystals, so-called otoconia, which are dislocated from the macula of the utricle mostly into the posterior semicircular canal. Free floating otoconia can move under the influence of gravity inside the semicircular canal (canalolithiasis) or adhere to the cupula (cupulolithiasis) causing displacement of the cupula. This results in positional nystagmus, whose directions and time courses are characteristic for the affected semicircular canal and the underlying cause. In recent years, however, a number of cases were reported, in which direction and times course of nystagmus differed from typical clinical findings. This may cause diagnostic problems., (© 2021. Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Benign paroxysmal positional vertigo (BPPV) is the most frequent form of vertigo seen in patients attending emergency departments. Leading symptoms are short attacks of vertigo provoked by head or body rotations. BPPV is caused by small calcium crystals, so-called otoconia, which are dislocated from the macula of the utricle mostly into the posterior semicircular canal. Free floating otoconia can move under the influence of gravity inside the semicircular canal (canalolithiasis) or adhere to the cupula (cupulolithiasis) causing displacement of the cupula. This results in positional nystagmus, whose directions and time courses are characteristic for the affected semicircular canal and the underlying cause. In recent years, however, a number of cases were reported, in which direction and times course of nystagmus differed from typical clinical findings. This may cause diagnostic problems., (© 2021. Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Background: Vestibular paroxysmia (VP) is defined as neurovascular compression (NVC) syndrome of the eighth cranial nerve (N.VIII). The aim was to assess the sensitivity and specificity of MRI and the significance of audiovestibular testing in the diagnosis of VP., Methods: 20 VP patients and, for control, 20 subjects with trigeminal neuralgia (TN) were included and underwent MRI (constructive interference in steady-state, time-of-flight MR angiography) for detection of a NVC between N.VIII and vessels. All VP patients received detailed audiovestibular testing., Results: A NVC of N.VIII could be detected in all VP patients rendering a sensitivity of 100% and a specificity of 65% for the diagnosis of VP by MRI. Distance between brain stem and compressing vessels varied between 0.0 and 10.2 mm. In 15 cases, the compressing vessel was the anterior inferior cerebellar artery (75%, AICA), the posterior inferior cerebellar artery in one (5%, posterior inferior cerebellar artery (PICA)), a vein in two (10%) and the vertebral artery (10%, VA) in another two cases. Audiovestibular testing revealed normal results in five patients (25%), a clear unilateral loss of audiovestibular function in nine patients (45%) and audiovestibular results with coinstantaneous signs of reduced and increased function within the same nerve in six patients (30%). From the 20 TN patients 7, (35%) showed a NVC of the N.VIII (5 AICA, 1 PICA, 1 vein)., Conclusions: Only the combination of clinical examination, neurophysiological and imaging techniques is capable of (1) defining the affected side of a NVC and to (2) differentiate between a deficit syndrome and increased excitability in VP.

Background: Because of its widespread accessibly, computed tomographic angiography (CT-A) is a promising technique in the detection of intracranial circulatory arrest in brain death (BD). Several studies assessed this tool, but neither have standardized evaluation parameters been developed nor has information about specificity become available., Methods: We conducted a prospective study between January 2008 and April 2012. Thirty patients were admitted to our University Hospital (16 men and 14 women; age, 18-88 years) and underwent CT-A scanning at two occasions: immediately after the first signs of loss of brain stem reflexes and after definitive determination of brain. The results of CT-A were compared with transcranial Doppler ultrasonography and electroencephalogram., Results: In 3 of 30 patients, we observed a termination of contrast flow at the level of the skull base and foramen magnum in arterial scanning series before the clinical determination of BD. After the clinical determination of BD, the opacification of all vascular territories in arterial phase scanning was found in one case, but venous phase scanning revealed no blood return in internal cerebral veins. In all other cases, contrast filling ceased at level of skull base or below. The specificity of CT-A in the detection of intracranial circulatory arrest was 90%, and sensitivity was 97%., Conclusion: CT-A is reliable and appropriate technical investigation to detect intracranial circulatory arrest in BD. The evaluation of contrast enhancement in arterial phase scanning seems to be more reliable than that in venous phase. An international consensus about a uniformly applied CT-A protocol for the evaluation of BD should be established.

Background: The prognosis of patients who are comatose after cardiopulmonary resuscitation (CPR) is poor but can be improved by mild therapeutic hypothermia. We studied the question whether the known, reliable indicators of a poor prognosis after CPR are also valid for patients treated with CPR and hypothermia., Methods: This review is based on a selective search of the PubMed database for recent articles on the assessment of prognosis in persons who are comatose after CPR and therapeutic hypothermia., Results: On the basis of 21 clinical trials, 4 of which yielded level I evidence, 9 level II evidence, and 8 level III evidence, the following were identified as reliable indicators of a poor prognosis: generalized myoclonus, bilateral absence of the pupillary light response or of the corneal reflex, bilateral absence of the cortical components of median nerve somatosensory evoked potentials, a burst-suppression or isoelectric EEG, continuous generalized epileptiform discharges, and an elevated serum concentration of neuron-specific enolase (with a higher cutoff value than for normothermic patients)., Conclusion: If the prognosis is poor, this should be thoroughly discussed with the patient's family, and the nature and extent of further intensive treatment should be reconsidered. The patient's wishes, if known, are paramount. Any decision to withhold care should be taken only if there are multiple concurrent indicators of a poor prognosis. If only one such indicator is present, or if the findings are inconsistent, such decisions should be postponed.

The perceived subjective visual vertical (SVV) is an important sign of a vestibular otolith tone imbalance in the roll plane. Previous studies suggested that unilateral pontomedullary brainstem lesions cause ipsiversive roll-tilt of SVV, whereas pontomesencephalic lesions cause contraversive roll-tilts of SVV. However, previous data were of limited quality and lacked a statistical approach. We therefore tested roll-tilt of the SVV in 79 human patients with acute unilateral brainstem lesions due to stroke by applying modern statistical lesion-behavior mapping analysis. Roll-tilt of the SVV was verified to be a brainstem sign, and for the first time it was confirmed statistically that lesions of the medial longitudinal fasciculus (MLF) and the medial vestibular nucleus are associated with ipsiversive tilt of the SVV, whereas contraversive tilts are associated with lesions affecting the rostral interstitial nucleus of the MLF, the superior cerebellar peduncle, the oculomotor nucleus, and the interstitial nucleus of Cajal. Thus, these structures constitute the anatomical pathway in the brainstem for verticality perception. Present data indicate that graviceptive otolith signals present a predominant role in the multisensory system of verticality perception.

Background: The use of technical aids to confirm brain death is a controversial matter. Angiography with the intra-arterial administration of contrast medium is the international gold standard, but it is not allowed in Germany except in cases where it provides a potential mode of treatment. The currently approved tests in Germany are recordings of somatosensory evoked potentials (SSEP), brain perfusion scintigraphy, transcranial Doppler ultrasonography (TCD), and electroencephalography (EEG). CT angiography (CTA), a promising new alternative, is being increasingly used as well., Methods: In a prospective, single-center study that was carried out from 2008 to 2011, 71 consecutive patients in whom brain death was diagnosed on clinical grounds underwent recording of auditory evoked potentials (AEP) and SSEP as well as EEG, TCD and CTA., Results: The validity of CTA for the confirmation of brain death was 94%; the validity of the other tests was: 94% for EEG, 92% for TCD, 82% for SSEP, and 2% for AEP. In 61 of the 71 patients (86%), the EEG, TCD and CTA findings all accorded with the clinical diagnosis. The diagnosis of brain death was established beyond doubt in all patients., Conclusion: In this study, the technical aids yielded discordant results in 14% of cases, necessitating interpretation by an expert examiner. The perfusion tests, in particular, can give false-positive results in patients with large cranial defects, skull fractures, or cerebrospinal fluid drainage. In such cases, electrophysiologic tests or a repeated clinical examination should be performed instead. CTA is a promising, highly reliable new method for demonstrating absent intracranial blood flow. In our view, it should be incorporated into the German guidelines for the diagnosis of brain death.

We report a case of eosinophilic meningitis due to Angiostrongylus cantonensis in a patient who returned from Thailand. The presence of a compatible epidemiologic history and eosinophilia in cerebrospinal fluid (CSF) lead to the diagnosis, which was confirmed by detection of specific antibodies. After treatment with albendazole and corticosteroids he recovered completely.

Numerous crossed brain stem syndromes have been described, especially in the nineteenth century. While these syndromes are passed on in neurological textbooks, their relevance in clinical neurology remains to be elucidated. To investigate the prevalence of classical crossed brain stem syndromes in clinical practice, we prospectively recruited 308 consecutive patients with signs and symptoms indicative of acute brain stem infarction. Standardized high-resolution MR imaging and multimodal electrophysiological brain stem testing were applied to localize the site of the acute lesion. We performed a computer-based correlation of clinical signs and symptoms of our patients to those reported in the original historical publications for more than 25 crossed brain stem syndromes. Fourteen cases matched the clinical criteria of Wallenberg's syndrome, two patients had Babinski-Nageotte's syndrome, two had Raymond-Cestan's, one showed Weber's, and one Claude's syndrome. All other tested syndromes were not present in the cohort. More than 20% of patients showed different, so far unnamed crossed symptom combinations. In conclusion, except for Wallenberg's syndrome, classical crossed brain stem syndromes do not seem to play a relevant role in clinical neurology. Other syndromes may serve as theoretical models only that illustrate possible neuroanatomical connections in the human brain stem. This is complicated, however, by considerable topographic and terminological inconsistencies.

The topodiagnostic implications of hemiataxia following lesions of the human brainstem are only incompletely understood. We performed a voxel-based statistical analysis of lesions documented on standardised MRI in 49 prospectively recruited patients with acute hemiataxia due to isolated unilateral brainstem infarction. For statistical analysis individual MRI lesions were normalised and imported in a three-dimensional voxel-based anatomical model of the human brainstem. Statistical analysis revealed hemiataxia to be associated with lesions of three distinct brainstem areas. The strongest correlation referred to ipsilateral rostral and dorsolateral medullary infarcts affecting the inferior cerebellar peduncle, and the dorsal and ventral spinocerebellar tracts. Secondly, lesions of the ventral pontine base resulted in contralateral limb ataxia, especially when ataxia was accompanied by motor hemiparesis. In patients with bilateral hemiataxia, lesions were located in a paramedian region between the upper pons and lower midbrain, involving the decussation of dentato-rubro-thalamic tracts. We conclude that ataxia following brainstem infarction may reflect three different pathophysiological mechanisms. (1) Ipsilateral hemiataxia following dorsolateral medullary infarctions results from a lesion of the dorsal spinocerebellar tract and the inferior cerebellar peduncle conveying afferent information from the ipsilateral arm and leg. (2) Pontine lesions cause contralateral and not bilateral ataxia presumably due to major damage to the descending corticopontine projections and pontine base nuclei, while already crossed pontocerebellar fibres are not completely interrupted. (3) Finally, bilateral ataxia probably reflects a lesion of cerebellar outflow on a central, rostral pontomesencephalic level.

There is a suprasegmental influence on the masseter reflex (MassR) in animals, which is mediated via the fifth nerve spinal nucleus (5SpN). Corresponding data in humans are lacking. Out of 268 prospectively recruited patients with clinical signs of acute brainstem infarctions, we identified 38 with magnetic resonance imaging (MRI)-documented unilateral infarcts caudal to the levels of the fifth nerve motor and main sensory nuclei. All had biplanar T2- and echo planar diffusion-weighted MRI and MassR testing. Five patients (13%) had ipsilateral MassR abnormalities. In all, the infarcts involved the region of the 5SpN. Patients with medullary infarcts involving the region of the 5SpN may thus have ipsilateral MassR abnormalities. This possibly represents an interruption of an excitatory projection mediated via the 5SpN to masseter motoneurons in the fifth nerve motor nucleus. MassR abnormalities with medullary lesions restrict the topodiagnostic value of the MassR.

Dizziness is not a unique clinical picture, but rather is the unspecific symptom of numerous diseases. Dizziness always develops when the real incoming vestibular, visual and somatosensory information contradict each other and the expected input signals. Disorders of the vestibular apparatus are the most frequent cause of dizziness; in contrast, cervicogenic causes play a secondary role. Dizziness syndromes usually have a favourable prognosis and can be successfully treated.

Background: There is only limited data on improvements of critical medical care is resulting in a better outcome of comatose survivors of cardiopulmonary resuscitation (CPR) with generalized myoclonus. There is also a paucity of data on the temporal dynamics of electroenephalographic (EEG) abnormalities in these patients., Methods: Serial EEG examinations were done in 50 comatose survivors of CPR with generalized myoclonus seen over an 8 years period., Results: Generalized myoclonus occurred within 24 hours after CPR. It was associated with burst-suppression EEG (n = 42), continuous generalized epileptiform discharges (n = 5), alpha-coma-EEG (n = 52), and low amplitude (10 microV <) recording (n = 1). Except in 3 patients, these EEG-patterns were followed by another of these always nonreactive patterns within one day, mainly alpha-coma-EEG (n = 10) and continuous generalized epileptiform discharges (n = 9). Serial recordings disclosed a variety of EEG-sequences composed of these EEG-patterns, finally leading to isoelectric or flat recordings. Forty-five patients died within 2 weeks, 5 patients survived and remained in a permanent vegetative state., Conclusion: Generalized myoclonus in comatose survivors of CPR still implies a poor outcome despite advances in critical care medicine. Anticonvulsive drugs are usually ineffective. All postanoxic EEG-patterns are transient and followed by a variety of EEG sequences composed of different EEG patterns, each of which is recognized as an unfavourable sign. Different EEG-patterns in anoxic encephalopathy may reflect different forms of neocortical dysfunction, which occur at different stages of a dynamic process finally leading to severe neuronal loss.

To investigate the incompletely understood somatotopical organization of the corticospinal tract in the human brainstem, we performed a voxel-based statistical analysis of standardized magnetic resonance scans of 41 prospectively recruited patients with pyramidal tract dysfunction caused by acute brainstem infarction. Motor hemiparesis was rated clinically and by the investigation of motor evoked potentials to arms and legs. Infarction affected the pons in 85% of cases. We found the greatest level of significance of affected brainstem areas between the pontomesencephalic junction and the mid pons. Lesion location was significantly more dorsal in patients with hemiparesis affecting more proximal muscles and was significantly more ventral in patients with predominantly distal limb paresis. Comparison of magnetic resonance lesion from patients with paresis predominantly affecting arm or leg did not show significant topographical differences. We conclude that a topographical arm/leg distribution of corticospinal fibers is abruptly broken down as the descending corticospinal tract traverses the pons. Corticospinal fibers, however, follow a somatotopical order in the pons with fibers controlling proximal muscles being located close to the reticular formation in the dorsal pontine base, and thus more dorsal than the fibers controlling further distal muscle groups.

Background: Small brainstem infarctions are increasingly recognized as a cause of isolated ocular motor and vestibular nerve palsies in diabetic and/or hypertensive patients. This raises the question whether there are also isolated 7(th) nerve palsies due to pontine infarctions in patients with such risk factors for the development of cerebrovascular diseases., Methods: Over an 11-year-period, we retrospectively identified 10 diabetic and/or hypertensive patients with isolated 7(th) nerve palsies and electrophysiological abnormalities indicating pontine dysfunction. All patients had examinations of masseter and blink reflexes, brainstem auditory evoked potentials, direct current electro-oculography including bithermal caloric testing, and T1- and T2-weighted MRI (slice thickness: 4-7 mm)., Results: Electrophysiological abnormalities on the side of the 7(th) nerve palsy included delayed masseter reflex latencies (4 patients), slowed abduction saccades (4 patients), vestibular paresis (2 patients), and abnormal following eye movements (2 patients). Electrophysiological abnormalities were always improved or normalized at re-examination, which was always associated with clinical improvement. MRI revealed an ipsilateral pontine infarction in 2 patients. Another 2 had bilateral hyperintense intrapontine lesions, and one an ipsilateral cerebellar infarction., Conclusions: Simultaneous improvement or recovery of abnormal clinical and electrophysiological findings strongly indicated that both were caused by the same actual pontine lesions. A 7(th) nerve palsy may be the only clinical sign of a pontine infarction in diabetic and/or hypertensive patients. Such mechanism may be underestimated if based on MRI only.

Burst-suppression EEG (BS-EEG) after cardiopulmonary resuscitation implies a bad prognosis, but little is known of the temporal dynamics of postanoxic BS-EEG. The authors studied 24 consecutive patients who developed BS-EEG within 24 hours after cardiopulmonary resuscitation, and followed 20 of these patients with serial EEGs. Except for one patient, BS-EEG was followed by another EEG pattern within 1 day, mainly areactive alpha EEG (n = 6), isoelectric EEG (n = 5), generalized continuous epileptiform discharges (n = 4), or theta; EEG (n = 3). The coexistence of different EEG patterns in the same recording was seen in 10 patients. Serial recordings disclosed a variety of EEG sequences with (often subtle) transitions between the different EEG patterns, including reappearance of BS-EEG. Postanoxic BS-EEG is followed by a variety of EEG sequences composed of different EEG patterns, each of which is recognized as an unfavorable sign in and of itself. The coexistence of different unfavorable EEG patterns in the same recording, and transitions between these EEG patterns in subsequent recordings, are common in patients with postanoxic BS-EEG. It seems reasonable to speculate that BS-EEG and subsequently evolving EEG patterns in anoxic encephalopathy reflect different forms of neocortical dysfunction, which occur at different stages of a dynamic process, leading ultimately to severe neuronal loss.

There is a significant number of individual patients with cranial nerve palsies as the sole manifestation of MRI- and, less frequently, CT-documented small brainstem infarctions or hemorrhages. The 3rd and 6th nerves are most commonly involved and, less frequently, the 4th, 5th, 7th, and 8th nerves. An intra-axial basis for such lesions may be underestimated if the diagnosis is based solely on MRI. The electrophysiologic abnormalities indicating brainstem lesions may be independent of MRI-documented morphological lesions. This paper reviews the literature on cerebrovascular brainstem diseases manifesting as isolated cranial nerve palsies. It supports the concept that small pontine and mesencephalic infarctions are the main cause of non-traumatic cranial nerve palsies in the middle-aged and elderly population. Microvascular infarction of the respective extra-axial cranial nerve segments seem to be less important., (Copyright 2002 S. Karger AG, Basel)