Recurrent stenosis following carotid artery stenting treated with a drug-eluting balloon: a single-center retrospective analysis.

PURPOSE: Early in-stent restenosis after stent-protected angioplasty of the carotid artery (SPAC) is an infrequent, but potentially harmful condition for patients with carotid artery disease. METHODS: In our retrospective single-center analysis of 176 patients with carotid artery stenting between 2009 and 2015, using duplex ultrasound, we detected 9 patients with high-grade carotid artery in-stent restenosis. All restenosis patients were treated with a drug-eluting balloon (DEB) to prevent recurrent neointimal hyperplasia. One patient had bilateral carotid artery disease with bilateral in-stent restenosis, and 1 patient needed repeated DEB treatment 19 months after the first DEB intervention, so 11 DEB procedures, in total, were performed. RESULTS: The median time-interval between primary carotid artery stenting and first DEB-treatment was 9 months. In 3 of the 11 interventions, the DEB treatment was assisted by an additional stent. One repeat DEB treatment was necessary, and three DEB treatments were followed by a secondary stent. No peri-interventional complications (TIA, stroke, or death) were observed during or after DEB intervention. Therefore, in the entire group, the 1y event-free survival (EFS) was 100%, and the 2y/3y/5y EFS was 83%. CONCLUSION: DEB intervention seems to be an effective and safe treatment for patients with high-grade in-stent restenosis after SPAC.

[Myasthenia gravis should be considered in cases of Parkinson's disease and progressive dysphagia]. / Bei Morbus Parkinson und progredienter Dysphagie an Myasthenia gravis denken.

We report on four consecutive patients with Parkinson's disease, in whom anti-acetylcholine receptor (AChR) antibody positive bulbar myasthenia gravis (MG) turned out to be responsible for progressive dysphagia.

[Slowly progressive dysarthria in primary lateral sclerosis]. / Langsam progressive Dysarthrophonie bei primärer Lateralsklerose.

Slowly progressive dysarthria over many years may be the only sign of primary lateral sclerosis (PLS). Clinically it presents as pseudobulbar palsy which can be differentiated from amyotrophic lateral sclerosis (ALS) by the longer disease duration (> or =4 years), central pathological magnetic-evoked potentials to the tongue and lack of denervation in EMG. In contrast, hereditary spastic paraplegia (HSP) is characterized by a primary spasticity of the lower limbs, mostly later onset, the fact that other family members are affected and in isolated cases by positive genetic testing for mutations.

[Central positional vertigo due to cerebellar nodular infarction]. / Lagerungsschwindel bei zerebellärem Nodulusinfarkt.

Nodular infarctions are a rare cause of vertigo and may imitate vestibular neuritis. We report on two patients with acute positional vertigo due to nodular infarction, a clinical presentation is not reported so far. High-resolution MR imaging using thin slices is required to identify isolated nodular infarctions.

Left-hemispheric dominance for articulation: a prospective study on acute ischaemic dysarthria at different localizations.

Dysarthria is a frequent symptom in cerebral ischaemia. However, speech characteristics of these patients have not previously been investigated in relation to lesion site in a prospective study. We investigated the auditory perceptual features in 62 consecutive patients with dysarthria due to a single, non-space-occupying cerebral infarction confirmed by MRI. Standardized speech samples of all patients were stored within 72 h after stroke onset using a digital tape recorder. Speech samples were assessed independently by two experienced speech therapists, who were unaware of the clinical and neuroradiological findings, using an interval scale ranging from 0 to 6. Separately assessed were features of articulation, phonation, prosody, and the global severity for a total of 31 items. Extracerebellar infarctions (85.5%) were located in the lower motor cortex (14.5%), striatocapsular region (46.8%) and base of the pons (24.2%). Isolated cerebellar infarctions were present in 14.5% of patients. There was a strong correlation between the findings of both examiners, showing identical scores, or only minor differences (<1 on the assessment scale) for 80% of all items. The average severity of dysarthria was 2.9 +/- 1.3. Articulatory abnormalities were the predominant deviation characteristics, affecting in particular the production of consonants. However, phonatory and prosodic abnormalities were also frequently observed speech characteristics. As revealed by factor analysis of speech characteristics the total severity of dysarthria was mainly influenced by the impairment of articulation. Speech parameters describing characteristics of articulation and prosody showed significant side-to-side and area differences, while this effect was lacking for any voice parameter. Left cerebral lesions showed a more severe overall impairment of speech and articulation, independent of lesion topography. Thirty-eight of 62 patients were available for follow-up. Speech evaluation showed normal speech within weeks in 15 out of 38 patients (39.5%). In the other 23 patients overall severity of dysarthria was mild. This is the first prospective study which describes speech characteristics of dysarthria due to acute unilateral cerebral infarctions. We could demonstrate that dysarthria in extracerebellar infarctions was more frequently caused by left-sided lesions and that the severity of dysarthria was more pronounced in left-sided lesions independent from lesion topography. All extracerebellar lesions were located along the course of the cortico-bulbar tract fibres. Compatible with a common pathophysiological basis of dysarthria in these patients, none of the 31 speech items differed significantly between subcortical and brainstem lesions.

Brainstem reflex circuits revisited.

Our current understanding of brainstem reflex physiology comes chiefly from the classic anatomical-functional correlation studies that traced the central circuits underlying brainstem reflexes and establishing reflex abnormalities as markers for specific areas of lesion. These studies nevertheless had the disadvantage of deriving from post-mortem findings in only a few patients. We developed a voxel-based model of the human brainstem designed to import and normalize MRIs, select groups of patients with or without a given dysfunction, compare their MRIs statistically, and construct three-plane maps showing the statistical probability of lesion. Using this method, we studied 180 patients with focal brainstem infarction. All subjects underwent a dedicated MRI study of the brainstem and the whole series of brainstem tests currently used in clinical neurophysiology: early (R1) and late (R2) blink reflex, early (SP1) and late (SP2) masseter inhibitory reflex, and the jaw jerk to chin tapping. Significance levels were highest for R1, SP1 and R2 afferent abnormalities. Patients with abnormalities in all three reflexes had lesions involving the primary sensory neurons in the ventral pons, before the afferents directed to the respective reflex circuits diverge. Patients with an isolated abnormality of R1 and SP1 responses had lesions that involved the ipsilateral dorsal pons, near the fourth ventricle floor, and lay close to each other. The area with the highest probabilities of lesion for the R2-afferent abnormality was in the ipsilateral dorsal-lateral medulla at the inferior olive level. SP2 abnormalities reached a low level of significance, in the same region as R2. Only few patients had a crossed-type abnormality of SP1, SP2 or R2; that of SP1 reached significance in the median pontine tegmentum rostral to the main trigeminal nucleus. Although abnormal in 38 patients, the jaw jerk appeared to have no cluster location. Because our voxel-based model quantitatively compares lesions in patients with or without a given reflex abnormality, it minimizes the risk that the significant areas depict vascular territories rather than common spots within the territory housing the reflex circuit. By analysing statistical data for a large cohort of patients, it also identifies the most frequent lesion location for each response. The finding of multireflex abnormalities reflects damage of the primary afferent neurons; hence it provides no evidence of an intra-axial lesion. The jaw jerk, perhaps the brainstem reflex most widely used in clinical neurophysiology, had no apparent topodiagnostic value, probably because it depends strongly on peripheral variables, including dental occlusion.

Mechanical Recanalization following i.v. Thrombolysis: A Retrospective Analysis regarding Secondary Hemorrhagic Infarctions and Parenchymal Hematomas.

Introduction. In acute stroke by occlusion of the proximal medial cerebral artery (MCA) or the distal internal carotid artery, intravenous thrombolysis is an established treatment. Another option is mechanical recanalization. It remains unclear if the combination of both methods poses an additional bleeding risk. The aim of this retrospective analysis is to determine the proportion of hemorrhagic infarctions and parenchymal hematomas. Methods. Inclusion criteria were an occlusion of the carotid T or proximal MCA treated with full dose thrombolysis and mechanical recanalization. 31 patients were selected. Devices used were Trevo, Penumbra Aspiration system, Penumbra 3D Retriever, and Revive. The initial control by computed tomography was carried out with a mean delay to intervention of 10.9 hours (SD: 8.5 hours). Results. A slight hemorrhagic infarction (HI1) was observed in 2/31 patients, and a more severe HI2 occurred in two cases. A smaller parenchymal hematoma (PH1) was not seen and a space-occupying PH2 was seen in 2/31 cases. There was no significant difference in the probability of intracranial bleeding after successful (thrombolysis in cerebral infarctions 2b and 3) or unsuccessful recanalization. Conclusion. The proportion of intracranial bleeding using mechanical recanalization following intravenous thrombolysis appears comparable with reports using thrombolysis alone.

Idiopathic trigeminal sensory neuropathy with gadolinium enhancement in the cisternal segment.

The authors report two patients with idiopathic trigeminal sensory neuropathy who showed gadolinium enhancement of the cisternal segment of the corresponding trigeminal nerve in cranial MRI. The resolution of these lesions in a repeat MRI suggests a similarity to Bell's palsy.

Dysarthria and lacunar stroke: pathophysiologic aspects.

We investigated the supranuclear tracts involved in speech production in 8 patients with dysarthria associated with a single lacunar stroke. Magnetic resonance imaging revealed the lesion site in 7 out of 8 patients. We tested corticobulbar tract function using transcranial magnetic stimulation and demonstrated impairment of the corticolingual projections in all the patients and in 5 patients impairment of the corticofacial projections. Sensory function in the oral cavity was impaired in 1 out of 8 patients. 99mTc hexamethyl-propylene amine oxime-single-photon emission computerized tomography (HMPAO-SPECT) imaging, performed in 5 patients, showed cerebellar diaschisis in 1, suggesting additional cerebropontocerebellar tract impairment. Dysarthria observed in the 2 patients with impaired sensation in the oral cavity or with cerebellar diaschisis did not differ from the dysarthria found in the other patients. We conclude that interruption of the corticolingual pathways to the tongue is crucial in the pathogenesis of dysarthria following extracerebellar lacunar stroke.

Isolated voluntary facial paresis due to pontine ischemia.

We describe a patient with isolated voluntary facial paresis due to a unilateral lacunar lesion in the contralateral mediodorsal middle base of the pons. Transcranial magnetic stimulation confirmed the involvement of supranuclear corticofacial tract fibers and sparing of the corticolingual and corticospinal connections. This observation demonstrates that the fibers conveying voluntary orofacial activation descend mediodorsally at the level of the middle pons and that the fibers conveying emotional activation may be assumed to converge below this level.

Dysarthria in acute ischemic stroke: lesion topography, clinicoradiologic correlation, and etiology.

BACKGROUND AND PURPOSE: Although dysarthria is a frequent symptom in cerebral ischemia, there is little information on its anatomic specificity, spectrum of associated clinical characteristics, and etiologic mechanisms. METHODS: An investigation of 68 consecutive patients with sudden onset of dysarthria due to a single infarction confirmed by MRI or CT was conducted. RESULTS: Dysarthria was associated with a classic lacunar stroke syndrome in 52.9% of patients. Isolated dysarthria and dysarthria-central facial and lingual paresis occurred in 2.9% (n = 2) and 10.3% (n = 7), respectively. Dysarthria-clumsy hand syndrome was observed in 11.7% (n = 8) of patients and associated with pure motor hemiparesis and/or ataxic hemiparesis in 27.9% (n = 19). The lesions were due to small-vessel disease in 52.9% (n = 36), to cardioembolism in 11.8% (n = 8), and to large-vessel disease in only 4.4% (n = 3) of cases. Infarctions were located in the lower part of the primary motor cortex (5.9%; n = 4), middle part of the centrum semiovale (23.5%; n = 16), genu and ventral part of the dorsal segment of the internal capsule (8.8%; n = 6), cerebral peduncle (1.5%; n = 1), base of the pons (30.9%; n = 21), and ventral pontomedullary junction (1.5%; n = 1). Isolated cerebellar infarctions affected the rostral paravermal region in the superior cerebellar artery territory. CONCLUSIONS: Extracerebellar infarcts causing dysarthria were located in all patients along the course of the pyramidal tract. This finding correlates with the frequent occurrence of associated pyramidal tract signs in 90.7% (n = 62) of patients. Isolated cerebellar infarcts leading to dysarthria were in all cases located in the territory of the superior cerebellar artery.

Sensitivity of transcranial magnetic stimulation of cortico-bulbar vs. cortico-spinal tract involvement in Amyotrophic Lateral Sclerosis (ALS).

BACKGROUND: An upper motor neuron (UMN) lesion in amyotrophic lateral sclerosis (ALS) is often difficult to identify because clinical signs may be discrete or masked by severe simultaneous LMN lesions. We compared the diagnostic sensitivity of transcranial magnetic stimulation (TMS) to cranial muscles and limb muscles in the detection of UMN lesions. DESIGN: We investigated corticobulbar and corticospinal tract function to the tongue/orofacial muscles and abductor digiti minimi/tibial anterior muscles with TMS in 51 patients with ALS to compare the diagnostic yield in the detection of UMN dysfunction. An UMN lesion was assumed when the following were found: the peripheral conduction time and amplitude of the M-wave were within the normal range, the response to cortical stimulation was absent, the TMS evoked/M-wave amplitude ratio was reduced, and the central motor conduction time or the interside difference was delayed (> mean+2.5 SD). RESULTS: On the basis of these criteria a UMN lesion to the orofacial muscles was identified in 24 patients (47%), to the tongue in 27 (53%), and to the upper and lower limbs in 13 (25%) and 22 patients (43%), respectively. Combined abnormalities from all sites increased the diagnostic yield to 39 patients (76%). TMS of the limb muscles confirmed a UMN lesion in only 15 (54%) of the 28 patients with clinically confirmed UMN involvement. This number increased to 23 patients (82%) if tongue and orofacial muscles were taken into acount. CONCLUSION: Our results indicate the early and in most cases subclinical corticobulbar tract involvement of the central motor pathways to the orofacial muscles and tongue in ALS. TMS of the tongue and orofacial muscles had a higher sensitivity in identifying UMN lesions than that of the upper and lower limbs.

Sonographic analysis of laryngeal elevation during swallowing.

BACKGROUND: Swallowing disorders are common symptoms in many neurological diseases. The aim of this pilot-study was to analyse vertical laryngeal excursion during swallowing non-invasively using ultrasound sonographic techniques in patients with dysphagia compared with healthy volunteers. METHODS: Data were obtained from 42 healthy volunteers (mean age: 57 +/- 19 years) and 18 patients (mean age: 63 +/- 8 years) with dysphagia due to different neurological diseases using a 7.5 MHz linear array probe, which was placed in longitudinal position above the larynx. This allowed visualization of the contour and the acoustic shadow of the hyoid bone and the thyroid cartilage. The distance between the hyoid bone and the upper end of the thyroid cartilage during laryngeal elevation was readily assessed by video-mode function. RESULTS: In healthy subjects we found a mean distance of 220 (+/- 30) mm at rest; the shortest distance during swallowing of 5 or 10 ml water was 85 (+/- 11) mm and represents a reduction of 61 % (+/- 3) under physiological conditions. The mean relative laryngeal elevation in the patients with neurogenic dysphagia was reduced to only 42 % (+/- 10) (p < 0.0001). CONCLUSIONS: Ultrasound is a viable and non-invasive method in the investigation of laryngeal elevation during swallowing. It allows direct visualization of impaired laryngeal motion in patients with neurogenic dysphagia.

Electrophysiological brainstem investigations in obstructive sleep apnoea syndrome.

Phasic inspiratory genioglossus activity prevents pharyngeal airway collapse in healthy subjects during sleep and is diminished or absent in obstructive sleep apnoea syndrome (OSAS), thus leading to pharyngeal obstruction. Case reports of OSAS after pontomedullary lesions indicate that impaired inspiratory genioglossal activity may result from brainstem lesions. We therefore investigated brainstem functions in 18 awake patients with OSAS using brainstem auditory evoked potentials, blink reflex, masseter reflex, masseter inhibitory reflex (in 11 of 18 patients), magnetic evoked potentials of the tongue and electrooculography with vestibular testing. Fifteen of 18 patients showed no electrophysiological abnormalities. One patient had a left pontine and two patients a bilateral pontomesencephalic lesion, although a causal connection with OSAS was not conclusively confirmed. Our results do not support the assumption of a relevant structural brainstem lesion in OSAS patients with normal neurological findings.

Ipsilateral facial weakness in upper medullary infarction-supranuclear or infranuclear origin?

We describe two patients with upper medullary infarctions showing ipsilateral facial weakness and relative sparing of the upper facial muscles. Electrophysiological follow-up using transcranial magnetic stimulation of the motor cortex in combination with stimulation of the peripheral facial nerve disclosed a supranuclear (corticofacial) tract lesion in one patient and a partial nuclear/infranuclear intra-axial facial nerve lesion in another.

Electrophysiological brain stem investigations in idiopathic narcolepsy.

Narcolepsy is associated with various rapid eye movement (REM) sleep abnormalities. Distinct brain stem areas seem to play a prominent role in REM sleep regulation. Recent magnetic resonance imaging (MRI) studies have led to conflicting findings concerning the presence of structural brain stem lesions in patients with idiopathic narcoleptic syndrome. However, multimodal electrophysiological brain stem investigations may reveal functional brain stem abnormalities even in the absence of MRI abnormality. Therefore we investigated brain stem function in 12 idiopathic narcoleptic patients by systematically studying tegmental brain stem pathways. All of the patients met the diagnostic criteria of the International Classification of Sleep Disorders, with typical changes in polysomnography and the multiple sleep latency test. Electrophysiological investigations comprised masseter reflex, blink reflex, masseter inhibitory reflex, early auditory evoked potentials and electrooculography with vestibular testing. In no patient were electrophysiological brain stem abnormalities observed. Our findings do not support the existence of a relevant brain stem lesion in narcoleptic patients with normal neurological status.