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[A case of upper brainstem infarction developing symptomatic narcolepsy after the administration of anti-convulsant drugs].

A 52-year-old woman, who had ischemic infarction in the ventral upper brainstem due to subarachnoid hemorrhage in October 1986, had recurrent sleep and cataplexy attacks from May 1987. She was receiving valproate and phenytoin daily since 1986. The diagnosis of narcolepsy was made based on the clinical symptoms and EEG findings showing REM sleep during a sleep attack. Both sleep and cataplexy attack increased in parallel with an increase of the dose of anti-convulsant drugs and disappeared immediately after the discontinuation of the treatment. The findings that suggest that the administration of anti-convulsant drug as well as the brainstem vascular lesion was deeply involved in the development of narcolepsy in this case.

Brain Stem↗

Intractable hiccup induced by brainstem lesion.

Four patients with brainstem lesions presented with intractable hiccup and mild to moderate neurological signs. Two of the patients had been initially diagnosed as having a psychogenic cause for their hiccup. Magnetic resonance imaging (MRI) demonstrated brainstem infarction in one case, tuberculoma at the junction of the medulla oblongata and the cervical spinal cord in two, and a vermian tuberculoma compressing the brainstem in one. The brainstem infarct and one of the medullary tuberculoma were not detected on high resolution enhanced computed tomography. The 3 patients with CNS tuberculoma were free of hiccup 1-5 months after antituberculous chemotherapy. It is proposed that hiccup is not an abnormal reflex, but a myoclonus generated by repetitive activity of the "inspiratory solitary nucleus" due to release of higher nervous system inhibitory/-regulatory control. The neuroanatomical network and the mechanisms underlying the formation of intractable hiccup are outlined. The value of MRI in the initial diagnosis and follow-up of patients with intractable hiccup due to brainstem lesions is emphasised.

Adult↗

Brainstem auditory evoked responses in brainstem infarction.

Brainstem auditory evoked responses (BAERs) were recorded in 40 patients with clinically definite brainstem infarction, and results were compared to localizations from physical signs and CT scans. The BAER was abnormal in 92% of patients with evidence on physical examination of dysfunction of lateral structures in the pons or midbrain. Normal BAERs were seen with medially-situated or medullary lesions. When both rostrocaudal level and lateralization were considered, the BAER indicated damage in additional areas not evident on physical examination in 25% of patients. However, physical signs indicated damage in areas not reflected by the BAER in 22% of patients. Therefore, the BAER complements the localization obtained from physical findings. BAERs were abnormal in more of these patients than were CT scans, and thus are useful for confirmation of bedside impressions.

Brain Stem↗

[Regressing median peduncular infarction].

A case of a medial and caudal infarction of the midbrain in a 56 years old woman is reported. The clinical syndrome included a rapidly recovering sleepiness, an ophthalmoplegia related to damage to the caudal part of the oculomotor nuclear complex, a slow extrapyramidal dysarthria and a severe ataxia. The latter was characterized by the prevalent involvement of posture control, resulting from an axial hypotonia and the lack of balance reflexes. The CT scan showed a low density area in the central part of the midbrain. Electrophysiological investigations were carried out to study the impairment of the sensory and auditory tracts in the brainstem. In spite of the gravity of initial signs, recovery was good and the patient led a normal life 8 months later.

Ataxia↗

Abeta-fiber mediated activation of cingulate cortex as correlate of central post-stroke pain.

A patient is presented who suffered a lateral brainstem infarction which selectively abolished pain and temperature sensitivity in the lower right limb. One year later central post-stroke pain had developed in the affected limb with touch and cold allodynia. P40m dipoles calculated from magnetoencephalographic fields after electrical stimulation of both tibial nerves were localized in SI as is seen in normal subjects. However, stimulation of the affected side caused deep pain sensations and elicited a large N80m component, best explained by an additionally active dipole in cingulate cortex. This early co-activation in a limbic structure suggests peripheral Abeta-fiber mediation and lemniscal projection. Abnormal link to the pain system may be due to sensitization and reorganization above the level of nociceptive deafferentation.

Brain Stem↗

[Subclinical attention changes in transient ischemic attacks in the vertebrobasilar region].

INTRODUCTION: A significant number of patients who have had cerebrovascular illness apparently recover their former abilities completely but return to normal life with subtle cognitive deficits which may affect their daily lives. Such is the situation of patients with transitory ischemic accidents who present with sustained, undiagnosed attention deficits. OBJECTIVES: To identify subclinical alterations due to attention deficits in patients with transitory ischemic accidents, and to contribute to the study of the physiopathological mechanisms involved in the integration of this function. PATIENTS AND METHODS: We examined 44 persons, divided into three groups for this study: one group had vertebro-basilar transitory ischemic accidents, a second group had supratentorial infarct and a third was healthy. All were given a specially designed computerized test of continuous work to evaluate the sustained attention component. RESULTS: Significant differences were found between the transitory ischemic accidents and healthy groups, regarding the variables including correct answers, omissions and indications of attention. This was not seen with the variables involving reaction time and number of errors. This demonstrated the existence of attention disorders involving omission in the group of patients with transitory ischemic accidents. CONCLUSION: These findings suggest the hypothesis that in the vertebro-basilar region there are important mechanisms involved in the process of sustained attention.

Acute Disease↗

Skew deviation with ocular torsion: a vestibular brainstem sign of topographic diagnostic value.

Fifty-six patients with unilateral brainstem infarctions presenting with skew deviation of the eyes were analyzed for static vestibular function in the roll plane. Ischemic lesions were allocated to the level and side of the brainstem by the clinical syndrome and neuroimaging. Two findings of clinical relevance were obtained: (1) All skew deviations were ipsiversive (ipsilateral eye was undermost) with caudal pontomedullary lesions and contraversive (contralateral eye was lowermost) with rostral pontomesencephalic lesions. (2) All skew deviations were associated with concomitant ocular torsion and tilts of subjective visual vertical toward the undermost eye. Thus, skew deviation or more correctly, ocular skew torsion is a sensitive brainstem sign of localizing and lateralizing value. Evidence is presented that the ocular skew torsion sign indicates a vestibular tone imbalance in the roll plane secondary to graviceptive pathway lesions.

Adolescent↗

[Experimental research on effect of human mesenchymal stem cells induced by shenqi fuzheng injection in cerebral infarction].

OBJECTIVE: To investigate the effect of shenqi fuzheng injection (SFI) in inducing differentiation of human mesenchymal stem cells (hMSCs) in brain stem and its effect on nervous function in model rats of cerebral infarction. METHODS: Middle cerebral artery occlusion model rats were made, and hMSCs was injected into their brain after being amplified in vitro and incubated with SFI for 0.5 h, then the survival, migration and differentiation of hMSCs in brain stem as well as the change of nervous function in model rats were observed. RESULTS: The post-transplantation reject reaction to hMSCs was low, it could survive as long as 6 weeks or more. No difference in area of infarction was shown before and after transplantation. Immunohistochemical staining showed that hMSCs expressed human neuron specific enolase (NSE), neurofilament (NF) and glial fibrillary acid protein (GFAP). The limb-kinetic function and tactile perception were improved in the model rats. CONCLUSION: SFI can induce hMSCs differentiate into neurons in vivo, and hMSCs may be the ideal germinal cells for treating cerebral infarction.

Animals↗

Watershed infarction of spinal cord after the embolization of bronchial artery: a case report.

A case of watershed infarction in the spinal cord is reported. The patient underwent bronchial artery embolization for control of massive hemoptysis. The bronchial arteriogram was carefully examined and focused on blood supply to the spinal cord prior to embolization. Acute paraparesis followed the embolization procedure even though there was no visible spinal supply on the arteriogram. Magnetic resonance imaging showed a hyperintensity lesion over the watershed region which is located at the central portion of the upper thoracic cord. This case is reported to emphasize the significant role which angiographically invisible small vessels can play in the blood supply to the spinal cord. The vascular system of the spinal cord and the prevention of spinal cord ischemia secondary to embolization are further discussed here.

Adult↗

Pathological eye-head coordination in roll: tonic ocular tilt reaction in mesencephalic and medullary lesions.

The fundamental pattern of coordinated eye-head roll motion is based upon utricular/saccular as well as vertical canal input, and mediated by the graviceptive pathways from the labyrinths via pontomedullary vestibular nuclei to the rostral midbrain tegmentum. The tonic bilateral graviceptive input stabilizes the eyes and head in the normal upright position. A unilateral lesion causes imbalance in vestibular tone in the roll plane which results in a tonic ipsiversive ocular tilt reaction (OTR). OTR, the triad of ipsilateral head tilt, skew deviation and ocular torsion, occurred as a tonic response (nonparoxysmal) persisting over months to years and was presumed to be due to upper brainstem lesions in 3 patients. Precise localization was limited because of the nature of the lesions. A reversible tonic OTR was seen with acute infarction of the dorsolateral medulla oblongata in 4 out of 11 patients. It may be explained by an ipsilateral lesion of the posterior canal pathways. Transient OTR seems not to be rare in acute Wallenberg's syndrome and ocular torsion in these patients is dysconjugate with predominant excyclotropia of the ipsilateral hypotropic eye. A deviation of the subjective visual vertical in the direction of the spontaneous head tilt--a previously undescribed feature of OTR--was present in all 7 patients and indicates a pathological shift of the internal representation of the gravitational vector. With respect to perception (subjective vertical) it is proposed that the manifest ipsiversive OTR represents a motor compensation of an apparent eye-head tilt contraversive to the lesioned side. Despite the resulting postural imbalance and the conflicting true vertical of the visual surround, the eyes, head and body are continuously adjusted to what the central nervous system erroneously computes as being vertical.

Adult↗

Positron emission tomography in diagnosing brainstem vascular lesions that cause abnormal eye movements.

PURPOSE: To evaluate the efficacy of positron emission tomography (PET) in aiding in the diagnosis of brainstem infarctions that cause abnormal eye movements. METHOD: Cerebral glucose metabolism was examined by PET with 18F-fluorodeoxyglucose as a tracer in five normal control subjects and six patients with abnormal eye movements. The PET images were registered to and superimposed on magnetic resonance images (MRIs). RESULTS: All control subjects showed little asymmetry of glucose metabolism in the brainstem, whereas all six patients demonstrated areas of low glucose metabolism in the brainstem. Areas of low metabolism seen by PET were wider than they appeared to be by MRI; MRIs even appeared normal in some patients. Asymmetry index measurements at the level of the ischemic lesion ranged between 19% and 45%. CONCLUSIONS: Positron emission tomography detected metabolic abnormality in patients with brainstem lesions that caused abnormal eye movements. Superimposing PET images on MRIs accurately localized abnormally low metabolism in the brainstem. Combined imaging with PET and MRI can be used to diagnose ischemic lesions in the brainstem from functional (PET) and morphologic (MRI) viewpoints.

Adult↗

[Localization of level of lesions in internuclear ophthalmoplegia through assessment of masseter and blink reflex].

The masseter and blink reflexes were investigated in 100 patients with internuclear ophthalmoplegia due to multiple sclerosis (58 patients) or lacunar brainstem infarction (42 patients). In unilateral internuclear ophthalmoplegia, 38 of 60 patients (63.3%) had masseter reflex abnormalities, two patients (3.3%) showed changes of the blink reflex R1 component, and 13 patients (21.7%) combined alterations of the masseter reflex and the blink reflex R1 component. 46 (86.8%) of these 53 patients with electrophysiological abnormalities had unilateral changes, which were ipsilateral to the medial longitudinal fasciculus lesion in 42 patients (91.3%). In bilateral internuclear ophthalmoplegia, 24 of 40 patients (60.0%) had abnormalities of the masseter reflex, two (5.0%) showed changes of the blink reflex R1, and nine (22.5%) combined alterations of the masseter reflex and the blink reflex R1 component. 20 (57.1%) of these 35 patients with electrophysiological abnormalities had bilateral changes. Thus, masseter reflex abnormalities indicating midbrain lesions were seen in 63.3% and 60.0%, respectively, of unilateral and bilateral internuclear ophthalmoplegia. Blink reflex R1 component changes with or without impairment of the masseter reflex indicating rostral pontine to midpontine lesions occurred in 25.0% and 27.5%, respectively. These figures correspond to the results of postmortem examinations and to theoretical considerations based on the length of the medial longitudinal fasciculus.

Adult↗

Impaired vasoreactivity of the basilar artery system in patients with brainstem lacunar infarcts.

BACKGROUND AND PURPOSE: Diminished vasoreactivity (VR) has been evidenced in patients with hemispheric small vessel disease, however, there is no data regarding vertebrobasilar (VB) territory VR changes in patients with subcortical vascular encephalopathy located in the brainstem. Therefore, we compared the cerebral blood flow velocity (CBFV) responses of the VB system during different vasoregulatory challenges in healthy volunteers to those in patients with brainstem lacunar infarcts. METHODS: In 20 patients with brainstem lacunar infarcts and in 10 healthy volunteers the VR of the VB system was measured by analyzing the CBFV changes during different stimulation paradigms (ventilation, tilting and acetazolamide tests). During transcranial Doppler registration the systemic blood pressure and the expiratory partial CO2 pressure were monitored. RESULTS: During hypercapnia the VR was significantly higher in the control group than in the patient group (10.1 +/- 4.9 vs. 3.4 +/- 5.0 cm/s/kPa, p = 0.0025). In a subgroup of patients with mean baseline CBFV <25 cm/s the VR was 1.5 +/- 2.4 cm/ s/kPa, while patients with mean baseline CBFV >25 cm/s showed a significantly higher value (7.8 +/- 6.9 cm/s/kPa). Furthermore, in patients with mean baseline CBFV <25 cm/s the pulsatility index was significantly higher than in patients with mean baseline CBFV >25 cm/s (1.11 +/- 0.26 vs. 0.86 +/- 0.19, p = 0.0325), reflecting significantly higher vascular resistance in the former group. Although CBFV measurements during tilting and acetazolamide tests tended to support these findings, they showed no significant differences between patients and controls. CONCLUSION: Patients with cerebral microangiopathy involving the brainstem showed impaired VR in the VB flow territory in association with baseline CBFV.

Acetazolamide↗

Mechanisms of dysphagia in suprabulbar palsy with lacunar infarct.

BACKGROUND AND PURPOSE: The objective of the present study was to investigate the neural mechanisms of dysphagia in suprabulbar palsy (SBP) with multiple lacunar infarct. METHODS: We evaluated the swallowing disorders of patients with SBP (n=34) and age-matched healthy control subjects (n=35) by means of an electrophysiological method that recorded the oropharyngeal swallowing patterns. With this method, dysphagia limit, the triggering of voluntarily initiated swallows, duration of laryngeal relocation time, and total duration of oropharyngeal swallowing were recorded and measured. In addition, the EMG behavior of the cricopharyngeal (CP) muscle of the upper esophageal sphincter was also assessed. RESULTS: In patients with SBP, the dysphagia limit in all except 1 patient was pathological with limits of <20-mL bolus volume, which is contrary to normal subjects, in whom the dysphagia limit exceeds the 20-mL bolus volume. Either triggering of swallowing reflex was delayed (P<0.04), or the swallow could hardly be triggered in 7 patients on the voluntary attempts for 3 mL water. Whenever the reflex swallowing could be triggered, it was slow and prolonged (P<0.01). The CP muscle of the upper esophageal sphincter appeared to have become hyperreflexic and incoordinated with laryngeal movements during swallowing. CONCLUSIONS: It was proposed that the progressive involvement of the excitatory and inhibitory corticobulbar fiber systems linked with the bulbar swallowing center is mainly responsible for the triggering difficulties of the swallowing reflex and for the hyperreflexic/incoordinated nature of the CP sphincter. In addition, the dysfunction of the extrapyramidal system has a specific role in the slowing of oropharyngeal swallowing and the accumulation of saliva in the mouth.

Adult↗

[A case of hemi-hyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction].

A case of hemihyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction is reported. A 55-year-old hypertensive man developed right hemiparesis with slight dysarthria and nausea upon awaking. The right side of his face and right upper limb and trunk to the level of the Th8-9 territory showed hyperhidrosis, which disappeared in a week. Ocular motor examination revealed that during forward gaze with the left eye fixing, the right eye deviated outward. The patient was able to adduct the right eye to midposition with the right eye fixing. Rightward gaze elicited full abduction and right-beating nystagmus of the right eye, but the left eye did not adduct. When he attempted to gaze leftward, both eyes made the full excursion, but saccades were slow in that direction. Convergence was intact. Vertical gaze was full, and he did not show Horner's sign. This ocular sign, non-paralytic pontine exotropia, disappeared three days later. T2-weighted spin echo magnetic resonance imaging disclosed a small lesion with high intensity in the inner side of the left middle pons. This hyperhidrosis was thought to be caused by destruction of inhibitory fibers thermoregulating sweating. These findings suggest that at the level of the middle pons inhibitory fibers descend along the inner side of facilitatory fibers thermoregulating sweating, which are speculated to descend the dorso-lateral part of the pontine tegmentum. These findings also suggest that lesions of non-paralytic pontine exotropia may be located in the paramedian pontine reticular formation rostral to the abducens nucleus with ipsilateral medial longitudinal fasciculus lesion, but further investigation is necessary.

Brain Stem↗

[Clinical aspects of brainstem infarction].

Ischemic stroke in the vertebrobasilar arterial territory often presents stunning signs and symptoms, and poses little difficulty in the clinical diagnosis. But in less dramatic cases, it is often difficult to make accurate clinical diagnosis and to document the precise extent of an infarct. The purpose of the present study is to demonstrate clinicotopographic correlations in patients with various brainstem and cerebellar infarctions and to reevaluate the importance of bedside clinical examinations for understanding pathophysiology and planning management of the patient. One hundred forty-three patients with clinical diagnosis of the vertebrobasilar infarction confirmed by MRI were studied. MRI is superior to CT scanning in delineating areas of infarction in the territory of posterior cerebral circulation because of the three dimensional approach and the lack of bone artifact. MRI also allowed very precise clinicotopographic correlations even in patients with good recovery, in whom pathologic verification of the lesion is not possible. There are some restrictions of MRI diagnosis to detect the clinical features which change from hour to hour, because of the mechanical limitation in spatial resolution and of the temporal uncertainty of the lesions such as reversible edema or coincidental asymptomatic old lesions. Clinical importance of ocular signs (eg. skew deviation, gaze limitations, nystagmus, pupillary abnormalities and so on) was discussed. Some eye-movement abnormalities (eg. gaze paresis, MLF syndrome, 'one-and-a-half' syndrome, lateropulsion or contrapulsion of eyes, and vertical nystagmus at the primary position) served as useful localizing signs, and especially their consecutive observations were of importance for clinical local diagnosis. Clinical syndromes, caused by lacunar lesions located either in the supratentorial or in the infratentorial structures, such as pure motor hemiparesis and ataxic hemiparesis were also discussed. In some cases of these syndromes, MRI failed to document the precise lesion responsible for the episode due to the multiplicities of small asymptomatic lesions. Even in such cases, detailed clinical informations (temporal profiles of the episode, past medical histories, neuro-ophthalmic signs and so on) may enable the differential diagnosis. It is concluded that the use of new imaging techniques such as MRI may provide new insights in the diagnosis of cerebrovascular diseases, but the importance of clinical observations can not be overemphasized.

Adult↗

[A case of brainstem infarction presenting with paralytic pontine exotropia and non-paralytic pontine exotropia].

We reported a patient with brainstem infarction who presented paralytic pontine exotropia (PPE) in acute phase and non-paralytic pontine exotropia (NPPE) during the recovery phase. On March 10, 1991, a 60-year-old man was brought to our hospital with chief complaints of double vision and right hemiparesis. The ocular position of the left eye on forward gaze was fixed at the midline, while the right eye was abducted, and skew deviation was observed. On leftward gaze, neither eye could pass the midline, and on rightward gaze the right eye was abducted and monocular nystagmus was noted in the abducted right eye, which indicated paralytic pontine exotropia. T2-weighted MRI showed high signal intensity lesions in the left paramedian portion of the mid-pontine tegmentum beneath the fourth ventricle, and in the midline of the pontine base extending to the left side. The next day, similar disturbance of ocular movement was seen on rightward gaze, but the limitation of leftward gaze had improved and NPPE was noted to have developed. On the third day, there was no abduction of the right eye on forward gaze, but left MLF syndrome was still present. Seven days later, the disturbances of ocular movement disappeared. The lesion was considered to be due to partial impairment of the left paramedian pontine reticular formation in addition to the MLF. PPE caused by ischemia due to the perforating arteries of the brainstem, different from that due to basilar artery occlusion may recover after progression through NPPE and MLF syndromes. Hence, one-and-a-half syndrome, PPE, NPPE, and MLF syndromes are considered to be analogous to one another.

Brain Stem↗

Sound lateralization and interaural discrimination. Effects of brainstem infarcts and multiple sclerosis lesions.

Subjects with brainstem lesions due to either an infarct or multiple sclerosis (MS) underwent two types of binaural testing (lateralization testing and interaural discrimination) for three types of sounds (clicks and high and low frequency narrow-band noise) with two kinds of interaural differences (level and time). Two major types of abnormalities were revealed in the lateralization performances: perception of all stimuli, regardless of interaural differences (time and/or level) in the center of the head (center-oriented), or lateralization of all stimuli to one side or the other of the head (side-oriented). Similar patterns of abnormal lateralization (center-oriented and side-oriented) occurred for MS and stroke patients. A subject's pattern of abnormal lateralization testing was the same regardless of the type of stimulus or type of interaural disparity. Lateralization testing was a more sensitive test than interaural discrimination testing for both types of subjects. Magnetic resonance image (MRI) scanning in three orthogonal planes of the brainstem was used to detect lesions. A semi-automated algorithm superimposed the auditory pathway onto each MRI section. Whenever a lesion overlapped the auditory pathway, some binaural performance was abnormal and vice versa. Given a lateralization test abnormality, whether the pattern was center-oriented or side-oriented was mainly determined by lesion site. Center-oriented performance was principally associated with caudal pontine lesions and side-oriented performance with lesions rostral to the superior olivary complex. For lesions restricted to the lateral lemniscus and/or inferior colliculus, whether unilateral or bilateral, just noticeable differences (JNDs) were nearly always abnormal, but for caudal pontine lesions JNDs could be normal or abnormal. MS subjects were more sensitive to interaural time delays than interaural level differences particularly for caudal pontine lesions, while stroke patients showed no differential sensitivity to the two kinds of interaural differences. These results suggest that neural processing of binaural stimuli is multilevel and begins with independent interaural time and level analyzers in the caudal pons.

Adult↗