P. P. Urban

Occurence and Clinical Predictors of Spasticity After Ischemic Stroke

Background and Purpose— There is currently no consensus on (1) the percentage of patients who develop spasticity after ischemic stroke, (2) the relation between spasticity and initial clinical findings after acute stroke, and (3) the impact of spasticity on activities of daily living and health-related quality of life. Methods— In a prospective cohort study, 301 consecutive patients with clinical signs of central paresis due to a first-ever ischemic stroke were examined in the acute stage and 6 months later. At both times, the degree and pattern of paresis and muscle tone, the Barthel Index, and the EQ-5D score, a standardized instrument of health-related quality of life, were evaluated. Spasticity was assessed on the Modified Ashworth Scale and defined as Modified Ashworth Scale >1 in any of the examined joints. Results— Two hundred eleven patients (70.1%) were reassessed after 6 months. Of these, 42.6% (n=90) had developed spasticity. A more severe degree of spasticity (Modified Ashworth Scale ≥3) was observed in 15.6% of all patients. The prevalence of spasticity did not differ between upper and lower limbs, but in the upper limb muscles, higher degrees of spasticity (Modified Ashworth Scale ≥3) were more frequently (18.9%) observed than in the lower limbs (5.5%). Regression analysis used to test the differences between upper and lower limbs showed that patients with more severe paresis in the proximal and distal limb muscles had a higher risk for developing spasticity (P≤0.001). Spasticity of the upper and lower limb was more frequent in patients with hemihypesthesia than in patients without sensory deficits (P≤0.001). Patients with spasticity showed a lower Barthel Index and EQ-5D score compared with the group without spasticity. Conclusions— Spasticity was present in 42.6% of patients with initial central paresis. However, severe spasticity was relatively rare. Predictors for the development of spasticity were a severe degree of paresis and hemihypesthesia at stroke onset.

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.

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

Different short-term modulation of cortical motor output to distal and proximal upper-limb muscles during painful sensory nerve stimulation

The pattern of upper‐limb muscle activation following painful stimulation has not been clarified in detail. We investigated the short‐term inhibitory and excitatory effects of painful electrical digital stimulation on the motoneuron pools of distal and proximal upper‐limb muscles. Transcranial magnetic stimulation (TMS) was used as test stimulus, and painful digital nerve stimulation as conditioning stimulus for motor evoked potential (MEP) recordings over the abductor digiti minimi (ADM), abductor pollicis brevis (APB), biceps brachii (BB), and deltoid muscles. Inhibition of the conditioned MEP response was most prominent in the distal muscles, whereas BB and deltoid muscles were only weakly inhibited. The mean MEP response over APB decreased with painful cutaneous stimuli, showing maximum inhibition (by 82%) at interstimulus intervals (ISIs) of 50 ms. Inhibition in the ADM was maximal (49%) but less pronounced at an ISI of 40 ms. The BB and deltoid muscles showed inhibition by 25% and 29%, respectively. Significant facilitation was present in BB and deltoid muscles by 43% and 41% at an ISI of 100 ms, but not in the smaller hand muscles. The observed pattern of upper‐limb muscle activation corresponds to the protective withdrawal reflex and the neuronal basis of the observed short‐term modulation of motor activity is compatible with a spinal or brainstem pathway. Muscle Nerve 29: 663–669, 2004

Sonographic analysis of laryngeal elevation during swallowing

Abstract.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.

Diffusion weighted magnetic resonance imaging in the diagnosis of reversible ischaemic deficits of the brainstem

Objectives: To evaluate the sensitivity of diffusion weighted magnetic resonance imaging (MRI) for the diagnosis of clinically suspected reversible ischaemic deficits of the brainstem. Methods: A total of 158 consecutive patients presenting with acute signs of brainstem dysfunction were investigated using EPI diffusion weighted MRI within 24 hours of the onset of symptoms. High resolution T1 and T2 weighted imaging was performed as a follow up after a median of six days Results: Fourteen of the 158 patients had a complete clinical recovery within 24 hours (transitory ischaemic attack (TIA)), and 19 patients recovered in less than one week (prolonged reversible neurological deficit (RIND)). Diffusion weighted MRI showed acute ischaemic deficits in 39% of patients with transient neurological deficits. The detection rate seemed to be higher in patients with longer lasting symptoms, but the difference between patients with TIA (29%) and RIND (47%) was not significant. Conclusions: Diffusion weighted MRI is a sensitive indicator of acute ischaemic brainstem deficits even in patients with reversible neurological deficit. Early identification of patients with TIA and increased risk of stroke may influence acute management and improve patient outcome.

Isolated dysarthria due to extracerebellar lacunar stroke: a central monoparesis of the tongue

OBJECTIVES The pathophysiology of dysarthria can preferentially be studied in patients with the rare lacunar stroke syndrome of “isolated dysarthria”. METHODS A single study was carried out on seven consecutive patients with sudden onset of isolated dysarthria due to single ischaemic lesion. The localisation of the lesion was identified using MRI. The corticolingual, cortico-orofacial, and corticospinal tract functions were investigated using transcranial magnetic stimulation. Corticopontocerebellar tract function was assessed using 99mTc hexamethylpropylene amine oxime-single photon emission computerised tomography (HMPAO-SPECT) in six patients. Sensory functions were evaluated clinically and by somatosensory evoked potentials. RESULTS Brain MRI showed the lesions to be located in the corona radiata (n=4) and the internal capsule (n=2). No morphological lesion was identified in one patient. Corticolingual tract function was impaired in all patients. In four patients with additional cortico-orofacial tract dysfunction, dysarthria did not differ from that in patients with isolated corticolingual tract dysfunction. Corticospinal tract functions were normal in all patients. HMPAO-SPECT showed no cerebellar diaschisis, suggesting unimpaired corticopontocerebellar tract function. Sensory functions were not affected. CONCLUSION Interruption of the corticolingual pathways to the tongue is crucial in the pathogenesis of isolated dysarthria after extracerebellar lacunar stroke.

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.

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.

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.99m Tc 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. NEUROLOGY 1996;47: 1135-1141