Frank Thömke

Observations on comatose survivors of cardiopulmonary resuscitation with generalized myoclonus

BackgroundThere 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.MethodsSerial EEG examinations were done in 50 comatose survivors of CPR with generalized myoclonus seen over an 8 years period.ResultsGeneralized 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 μV <) 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.ConclusionGeneralized 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.

Pontine lesions mimicking acute peripheral vestibulopathy

OBJECTIVES Clinical signs of acute peripheral vestibulopathy (APV) were repeatedly reported with pontine lesions. The clinical relevance of such a mechanism is not known, as most studies were biased by patients with additional clinical signs of brainstem dysfunction. METHODS Masseter reflex (MassR), blink reflex (BlinkR), brainstem auditory evoked potentials (BAEPs), and DC electro-oculography (EOG) were tested in 232 consecutive patients with clinical signs of unilateral APV. RESULTS Forty five of the 232 patients (19.4%) had at least one electrophysiological abnormality suggesting pontine dysfunction mainly due to possible vertebrobasilar ischaemia (22 patients) and multiple sclerosis (eight patients). MassR abnormalities were seen in 24 patients, and EOG abnormalities of saccades and following eye movements occurred in 22 patients. Three patients had BlinkR-R1 abnormalities, and one had delayed BAEP waves IV and V. Clinical improvement was almost always (32 of 34 re-examined patients) associated with improvement or normalisation of at least one electrophysiological abnormality. Brain MRI was done in 25 of the 44 patients and confirmed pontine lesions in six (two infarcts, three inflammations, one tumour). CONCLUSIONS Pontine dysfunction was suggested in 45 of 232 consecutive patients with clinical signs of APV on the basis of abnormal electrophysiological findings, and was mainly attributed to brainstem ischaemia and multiple sclerosis. The frequency of pontine lesions mimicking APV is underestimated if based on MRI established lesions only.

Isolated cranial nerve palsies in multiple sclerosis

During a 10 year period 24 patients with definite multiple sclerosis with isolated cranial nerve palsies were studied (third and fourth nerve: one patient each, sixth nerve: 12 patients, seventh nerve: three patients, eighth nerve: seven patients), in whom cranial nerve palsies were the presenting sign in 14 and the only clinical sign of an exacerbation in 10 patients. MRI was carried out in 20 patients and substantiated corresponding brainstem lesions in seven patients (third nerve: one patient, sixth nerve: four patients, eighth nerve: two patients). Additional abnormal findings of electro-oculography, or masseter reflex, or blink reflex, or combinations of these were found in 20 patients and interpreted in favour of a brainstem lesion at the level of the respective cranial nerve. In 11 of 14 patients with isolated cranial nerve palsies as the presenting sign of multiple sclerosis, dissemination in space was documented by MRI, and in the remaining three by evoked potentials. In patients with multiple sclerosis with isolated cranial nerve palsies, MRI is the most sensitive method of documenting dissemination in space and electrophysiological testing the most sensitive at disclosing brainstem lesions.

Mechanisms and predictors of chronic facial pain in lateral medullary infarction.

The purpose of this study was to identify clinical predictors and anatomical structures involved in patients with pain after dorsolateral medullary infarction. Eight out of 12 patients (67%) developed poststroke pain within 12 days to 24 months after infarction. The pain occurred in the ipsilateral face (6 patients) and/or the contralateral limbs and trunk (5 patients, 3 of whom also had facial pain). Ipsilateral facial pain was significantly correlated with lower medullary lesions, including those of the spinal trigeminal tract and/or nucleus, as documented by magnetic resonance imaging. The R2 blink reflex component was abnormal only in patients with facial pain. Likewise, pain and temperature sensation in the ipsilateral face was decreased in all patients with facial pain but not in patients without pain. Ipsilateral touch sensation in the face was also decreased in all patients with facial pain, but the lesions revealed on magnetic resonance imaging did not involve the principal sensory nucleus of the fifth cranial nerve, and the R1 blink reflex latencies were normal. Although facial pain was correlated with lesions of the spinal trigeminal tract and/or nucleus, none of the lesions involved the subnucleus caudalis, which contains most nociceptive neurons. These findings suggest that facial pain after medullary infarction is due to lesions of the lower spinal trigeminal tract (axons of primary afferent neurons), leading to deafferentation of spinal trigeminal nucleus neurons. Ann Neurol 2001;49:493–500

Symmetrical infarction of the cervical spinal cord due to spontaneous bilateral vertebral artery dissection.

To the Editor: Vertebral artery (VA) dissection is a well-known cause of vertebrobasilar ischemia in young people and may be due to preceding chiropractic maneuvers, cystic medial necrosis, mucopolysaccharidosis and reticular fiber diseases, vasculitis,1 2 or a yet-unknown arteriopathy.3 Common findings in VA dissection are unilateral or bilateral neck pain associated with cerebellar and brain stem (usually medullary) infarctions,2 3 which are rarely associated with clinical signs of spinal cord lesions.4 5 6 Recently, 1 patient each was described with bilateral spinal cord infarction7 and Brown-Sequard’s syndrome8 as the sole manifestation of spontaneous unilateral VA dissection. We add another patient with spontaneous bilateral VA dissection causing MRI-documented bilateral cervical cord infarction without clinical, electrophysiological, or radiological signs …

A topodiagnostic investigation on body lateropulsion in medullary infarcts

Body lateropulsion may occur without signs of vestibular dysfunction and vestibular nucleus involvement. The authors examined 10 such patients with three-dimensional brainstem mapping. Body lateropulsion without limb ataxia reflected an impairment of vestibulospinal postural control caused by a lesion of the descending lateral vestibulospinal tract, whereas body lateropulsion with limb ataxia was probably the consequence of impaired or absent proprioceptive information caused by a lesion of the ascending dorsal spino-cerebellar tract.

Evaluation of carpal tunnel syndrome in patients with polyneuropathy

The difference between the median nerve latency to the second lumbrical muscle and the ulnar nerve latency to the second interosseous muscle (L‐I DIFF) was tested in a prospective study to discriminate whether prolonged distal motor latency of the median nerve in patients with polyneuropathy (PNP) reflects an additional carpal tunnel syndrome (CTS). We investigated 92 patients (107 hands) with CTS, 30 patients (34 hands) with PNP, 22 patients (27 hands) with CTS and coexisting PNP (PNP+CTS), and 77 controls (87 hands). L‐I DIFF was significantly prolonged in both the CTS and PNP+CTS patients as compared to PNP patients and controls. It proved to be the most specific test to differentiate between diffuse (PNP) and focal (entrapment) nerve disorder.

The risk of abducens palsy after diagnostic lumbar puncture

Abducens palsy occasionally has been observed after diagnostic lumbar puncture (DLP).1-3 Its risk is not exactly known. We are aware of only one report, which mentions not a single case among 1,341 DLPs when using 22-gauge needles.4 At our clinic, an average of 800 inpatients a year undergo DLP. We usually use 22-gauge needles, and occasionally (in less than 5%), 20-gauge needles. Over a 14.5-year period, we saw two patients with abducens palsy—one unilateral, one bilateral—after DLP. This translates to a risk of less than 1 out of 5,800 DLPs. ### Patient 1. A 61-year-old man with type 2 diabetes noticed progressive weakness of the legs. Neurologic examination revealed proximal paraparesis, loss of deep tendon reflexes of the legs, diminished sensation to touch and pain in a stocking-like pattern, and diminished vibration sense. Nerve conduction studies documented sensorimotor demyelinating neuropathy of the legs and, less pronounced, of the …

Cerebrovascular Brainstem Diseases with Isolated Cranial Nerve Palsies

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.

MRI and neurophysiology in vestibular paroxysmia: contradiction and correlation

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.