[The chronically dizzy patient].

Many medical, neurologic and psychiatric conditions as well as drugs can give chronic dizziness, and a systematic diagnostic workup is essential. Chronic vestibular syndrome is a clinical syndrome of chronic vertigo, dizziness or unsteadiness lasting months to years. There is generally a persistent unilateral or bilateral vestibular loss. Treatment depends on the aetiology, but in general, treatment with vestibular rehabilitation is effective, which is summarised in this review. Betahistin or other anti-vertigo-drugs are not indicated in the treatment of chronic vertigo.

[Episodic vestibular syndrome].

Dizziness and vertigo are frequent symptoms in the primary care facility and emergency departments. Episodic vestibular syndrome (EVS) is defined as episodic dizziness, vertigo or postural imbalance with remission between episodes. EVS can be divided into spontaneous (s-EVS) and triggered EVS (t-EVS). Causes of s-EVS are vestibular migraine, Menière's disease, transient ischaemic attack and vestibular paroxysmia. Causes of t-EVS are benign paroxysmal positionel vertigo, orthostatic hypotension and panick attacks. In this review, we recommend using vestibular syndromes in order to reduce the number of differential diagnoses.

[Serotonin syndrome shortly after the administration of low-dose mirtazapine].

Serotonin syndrome is a rare neuropsychiatric complication caused by serotonergic drugs. Symptoms include confusion, psychosis, tremor, palpitations, hyperthermia, and the neurological examination shows signs of central nervous system deficits. This is a case report of a 67-year-old woman, who developed serotonin syndrome in the form of delusions, tremor, cerebellar ataxia and upper neuron signs one day after administration of low-dose mirtazapine therapy. Complete symptom remission occurred one week after the discontinuation of mirtazapine.

Ross Syndrome: A Patient with a 23-Year History.

We present a 60-year-old female with a 23-year history of anhidrosis with concomitant heat intolerance. At examination, we found a right-sided tonic pupil, absent tendon reflexes, and a segmental patch of compensatory hyperhidrosis in the left lower quadrant of her trunk. To further confirm this finding, a minor test (a starch-iodine test, which is used to evaluate the sudomotor function, sweating) was performed. Nerve conduction studies revealed evidence of a mild distal sensory polyneuropathy of the axonal type. Tilt-table testing showed signs of orthostatic hypotension with evidence of reduced sympathetic function. Skin biopsy excluded pathology in the sweat glands. Our patient met the criteria for a diagnosis of Ross syndrome. This case describes the long-term outcome of this rare entity and highlights how careful examination and bedside autonomic testing can confirm the diagnosis of autonomic neurological disorders.

Plasma-lactate levels in simulated seizures - An observational study.

PURPOSE: Differentiating between epileptic seizures, convulsive syncope or non-epileptic seizures is a common diagnostic challenge in the acute setting. Plasma-lactate levels have previously been proposed as a tool to aid in differentiating between epileptic and non-epileptic seizures, with lower levels of lactate suggesting a non-epileptic origin. The aim of this study was to investigate levels of lactate in non-epileptic seizures. METHODS: Healthy subjects were asked to perform a simulated seizure lasting no more than 5 min. Venous blood samples were taken before and immediately after the simulated seizure and analyzed using an ABL90 FLEX yielding information about lactate, pH, pO2,pCO2, electrolytes and plasma glucose. RESULTS: 8 people participated in the study: 6 men and 2 women aged 27-45. The average pre-simulation lactate was 1.1 mmol/L while the average pH was 7.39. The average post-simulation lactate was 10.2 mmol/L while the average pH was 7.25. This means an average increase in plasma-lactate of 9.1 mmol/L and an average drop of 0.15 in pH. CONCLUSION: Our data indicate that high rises in lactate levels are not specific for an epileptic origin. Further study of lactate as a marker for epileptic seizures is warrented.

Metronidazole-induced encephalopathy: a systematic review.

BACKGROUND AND AIMS: Metronidazole, a commonly used antibiotic drug, can cause adverse effects in the central nervous system termed metronidazole-induced encephalopathy, leading to diagnostic challenges. The condition is rare and a detailed description of its phenotype is lacking. In this systematic review we investigated the clinical features of metronidazole-induced encephalopathy to promote recognition and elaborate the description. METHODS: We performed a systematic literature search using PubMed.gov and hand searched the reference lists of included articles and other publications of interest. We included case series and single reports describing individual patients developing symptoms from the central nervous system in relation to metronidazole treatment. Data were extracted and analyzed descriptively. RESULTS: We identified 779 publications of which 112 papers comprising 136 patients were included. Typical findings were dysarthria, gait instability, limb dyscoordination and altered mental status. Frequently, patients concomitantly presented with metronidazole-induced polyneuropathy. Liver disease was the most common pre-existing condition. MRI showed a characteristic pattern of reversible symmetrical hyperintense lesions on T2/FLAIR of the dentate nuclei in 90% of patients. Most patients improved significantly after discontinuation of metronidazole. Poor outcome was associated with severe comorbidity. CONCLUSION: Metronidazole-induced encephalopathy should be considered in patients presenting with neurological symptoms in relation to newly initiated or prolonged metronidazole treatment. MRI changes are highly characteristic and specific. Patients with liver disease are at increased risk. Prognosis is good if recognized early.

[HINTS for diagnosing acute dizzy patients].

Acute vestibular syndrome (AVS) is an acute-onset of continuous vertigo with no other neurological deficits. AVS is most often of peripheral origin - vestibular organ or nerve. However, in some cases AVS is caused by a posterior circulation stroke (PCS). Head impulse, nystagmus and test of skew (HINTS) can be used to differentiate peripheral causes of AVS from central causes. Within the first 48 hours after onset of symptoms, HINTS has a higher sensitivity of detecting PCS (96-100%) than an MRI (72-87%). We recommend using HINTS for acute dizzy patients.

Convulsive Seizures as Presenting Symptom of Metronidazole-Induced Encephalopathy: A Case Report.

INTRODUCTION: Encephalopathy and convulsive seizures are rare manifestations of metronidazole toxicity. The incidence is unknown, but the condition has most frequently been reported in patients in their fifth to sixth decades. Usually, this condition is regarded as reversible, but permanent deficits and even death have been reported. CASE REPORT: A 66-year-old female patient undergoing metronidazole treatment for pleural empyema was admitted to our institution after her second episode of seizure. Over the course of 1 week after admittance, the patient developed several convulsive seizures along with progressive cerebellar dysfunction and cognitive impairment. MRI revealed bilateral, symmetrical hyperintense signal changes in the pons and dentate nuclei. EEG, ECG, lumbar puncture, and blood samples were normal. The patient improved already 2-3 days after discontinuation of metronidazole and was discharged fully recovered after 17 days. Follow-up clinical assessment and MRI were unremarkable. CONCLUSION: Metronidazole-induced encephalopathy is a rare condition, and due to a general lack of awareness the diagnosis is often delayed. This condition should be considered in metronidazole-treated patients presenting with unprovoked seizures, myoclonus, cerebellar signs, and encephalopathy. Characteristic MRI lesions may support the clinical suspicion.

Early trigeminal nerve involvement in Listeria monocytogenes rhombencephalitis: case series and systematic review.

Listeria monocytogenes is associated with rhombencephalitis. However, the exact mechanisms of brainstem invasion remains poorly understood. Here, we demonstrate clinical and radiological data suggesting that Listeria may invade the brainstem via the trigeminal nerve. Three females (41, 64 and 70 years) with culture proven L. monocytogenes bacteremia and rhombencephalitis were investigated in the period of 2014-16. T2-weighted and contrast-enhanced T1-weighted MRI revealed a cerebellopontine abscess in all three patients, including the involvement of the trigeminal nerve root. In two patients, MRI also revealed selective contrast enhancement of the sensory trigeminal tract in the pons and medulla oblongata. Prior to any other neurological symptoms, two patients complained of hypoesthesia and a tingling sensation in the ipsilateral half of the face, consistent with sensory trigeminal nerve dysfunction on that side. In addition, we identified another 120 cases of Listeria rhombencephalitis following a systematic review. Cranial nerves VII, V, IX, and X, respectively, medulla oblongata, cerebellum and pons, were the most frequently involved brain structures. The present clinical and radiological findings corroborate earlier data from animal experiments, indicating that L. monocytogenes may be capable of retrograde intra-axonal migration along the cranial nerves. We suggest that in a subset of patients with rhombencephalitis L. monocytogenes enters the cerebellopontine angle through the trigeminal nerve, invading the brainstem via the sensory trigeminal nuclei.

Widespread inflammation in CLIPPERS syndrome indicated by autopsy and ultra-high-field 7T MRI.

OBJECTIVE: To examine if there is widespread inflammation in the brain of patients with chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) syndrome by using histology and ultra-high-field MRI at 7.0T. METHODS: We performed a detailed neuropathologic examination in 4 cases, including 1 autopsy case, and studied 2 additional patients by MRI at 7.0T to examine (1) extension of inflammation to areas appearing normal on 3.0T MRI, (2) potential advantages of 7.0T MRI compared to 3.0T MRI in reflecting widespread inflammation, perivascular pathology, and axonal damage, and (3) the possibility of lymphoma. RESULTS: In the autopsy case, perivascular inflammation dominated by CD4+ T cells was not only detected in the brainstem and cerebellum but also in brain areas with normal appearance on 3.0T MRI, including supratentorial regions and cranial nerve roots. There was no evidence of lymphoma in any of the 4 patients. The 7.0T MRI in clinical remission also revealed supratentorial lesions and perivascular pathology in vivo with contrast-enhancing lesions centered around a small venous vessel. Ultra-high-field MRI at 7.0T disclosed prominent T1 hypointensities in the brainstem, which were not seen on 3.0T MRI. This corresponded to neuropathologic detection of axonal injury in the autopsy case. CONCLUSION: Our findings suggest more widespread perivascular inflammation and postinflammatory axonal injury in patients with CLIPPERS.

[Severe dysautonomy as a result of intra-cranial bleeding can cause an electrical storm with auricular fibrillation]. / Svær dysautonomi som følge af intrakranial blødning kan udløse elektrisk storm med ventrikelflimren.

A 69-year-old woman with a medical history of stroke and an ICD device due to torsade de pointes was admitted with a right basal ganglia haemorrhage. In the hours after admission the patient's condition severely declined and she developed fever, hypertension and flushing consistent with autonomic dysfunction with sympathetic storming. ICD interrogation revealed electrical storm with 138 appropriate shocks delivered at the night of admission. We wish to draw attention to the close link between brain and heart, which in predisposed patients with a new stroke can cause malignant arrhythmias.

Superior Orbital Fissure Syndrome and Ophthalmoplegia Caused by Varicella Zoster Virus with No Skin Eruption in a Patient Treated with Tumor Necrosis Alpha Inhibitor.

Varicella zoster virus lies dormant in the dorsal root ganglia after symptomatic chicken pox infection, usually in childhood. If the virus reactivates in the trigeminal ganglia, it can cause varicella zoster ophthalmicus, which can have severe ocular complications. We report a case of a 73-year-old woman in severe immunosuppression due to treatment with mycophenolate mofetil, glucocorticosteroids and a tumor necrosis factor alpha inhibitor. The reactivation caused superior orbital fissure syndrome, which has only rarely been described in relation to varicella zoster virus reactivation. In our case, the syndrome was seen along with severe encephalitis.

Diagnostic and therapeutic challenges in superficial CNS siderosis.

INTRODUCTION: Superficial CNS siderosis was previously almost unknown but is now diagnosed with increasing frequency owing to magnetic resonance imaging. Patients may present with sensory deafness, gait ataxia, various sensorimotor signs and, eventually, cognitive decline. They typically have a history of traumatic brain or spinal cord injury or previous neurosurgery, or may harbour congenital malformations. However, knowledge about treatment outcomes remains scarce. METHODS: We present a series of nine consecutive patients from a large tertiary neuroscience centre in order to highlight the challenges related to the diagnosis and treatment of superficial siderosis. RESULTS: A potential bleeding aetiology was identified in all patients, but removal of the offending bleeding source was achieved only in three (33%). Symptom progression was halted in just one patient (11%), which suggests that neurodegeneration due to haemosiderin-associated iron toxicity becomes irreversible with time. CONCLUSION: Surgical therapy in superficial CNS siderosis is rarely achieved. We suggest that prospective, large-scale multicentre studies are needed to search for non-surgical therapies that reverse (or prevent) ongoing neurotoxicity due to accumulating iron toxicity. FUNDING: not relevant. TRIAL REGISTRATION: not relevant.

[Myopathy and rhabdomyolysis after treatment with simvastatin, amlodipine, and roxithromycin].

This is a case report of a 71-year-old male with known diabetes, hypertension and diabetic nephropaty who over the course of one year developed an unrecognized myopathy due to concomitant treatment with high-dose simvastatin and amlodipin. Due to rhabdomyolysis he was after seven days of treatment with roxithromycin admitted to hospital with loss of the ability to walk. We wish to raise awareness of the potentially severe side effects of simvastatin and to emphasize that these can be limited by increased attention to patients with risk factors and to interactions with other drugs.