Paramedian Tegmentum Research Articles

Eight-and-a-half syndrome – A rare presentation of pontine infarction

Eight-and-a-half syndrome is clinically characterized by conjugate gaze palsy and internuclear ophthalmoplegia along with lower motor neuron type facial nerve palsy. Usually, it occurs because of infarction or demyelinating disease at paramedian tegmentum of lower pons. It emphasizes the importance of checking ocular movements. A 55-year-old male patient presented with sudden onset of double vision, headache, and vomiting and found to have horizontal gaze palsy, internuclear ophthalmoplegia, and facial palsy of the left side. High blood pressure was noted. Clinically, eight and a half syndrome was identified. MRI brain showed infarct at pons. The patient was stabilized systemically. A detailed clinical neuro-ophthalmic examination, along with a clear understanding of the neuro-anatomical pathways, gives clinicians a good diagnostic opportunity to localize precisely lesions in the brainstem. The disease should be evaluated for etiology.

Neuro-Ophthalmologic Features and Outcomes of Thalamic Infarction: A Single-Institutional 10-Year Experience.

Neuro-ophthalmologic deficit after thalamic infarction has been of great concern to ophthalmologists because of its debilitating impacts on patients' daily living. We aimed to describe the visual and oculomotor features of thalamic infarction and to delineate clinical outcomes and prognostic factors of the oculomotor deficits from an ophthalmologic point of view. Clinical and neuroimaging data of all participants were retrospectively reviewed. Among the 12,755 patients with first-ever ischemic stroke, who were registered in our Stroke Data Bank between January 2009 and December 2018, 342 were found to have acute thalamic infarcts on MRI, from whom we identified the patients exhibiting neuro-ophthalmologic manifestations including visual, oculomotor, pupillary, and eyelid anomalies. Forty (11.7%) of the 342 patients with thalamic infarction demonstrated neuro-ophthalmologic manifestations, consisting of vertical gaze palsy (n = 19), skew deviation with an invariable hypotropia of the contralesional eye (n = 18), third nerve palsy (n = 11), pseudoabducens palsy (n = 9), visual field defects (n = 7), and other anomalies such as isolated ptosis and miosis (n = 7). Paramedian infarct was the most predominant lesion of neuro-ophthalmologic significance, accounting for 84.8% (n = 28) of all patients sharing the oculomotor features. Although most of the patients with oculomotor abnormalities rapidly improved without sequelae, 6 (18.2%) patients showed permanent oculomotor deficits. Common clinical features of patients with permanent oculomotor deficits included the following: no improvement within 3 months, combined upgaze and downgaze palsy, and the involvement of the paramedian tegmentum of the rostral midbrain. Thalamic infarction, especially in paramedian territory, can cause a wide variety of neuro-ophthalmologic manifestations, including vertical gaze palsy, skew deviation, and third nerve palsy. Although most oculomotor abnormalities resolve spontaneously within a few months, some may persist for years when the deficits remain unimproved for more than 3 months after stroke.

Internuclear ophthalmoplegia plus ataxia indicates a dorsomedial tegmental lesion at the pontomesencephalic junction.

Internuclear ophthalmoplegia (INO) indicates a lesion involving the medial longitudinal fasciculus (MLF) that interconnects the abducens nucleus and medial rectus subnucleus of the oculomotor nuclear complex. In fact, rostral-caudal localization value of the INO is often limited except when it accompanies symptoms and signs owing to involvement of nearby structures. Ataxia is often observed in lesions involving the cerebellum or the fibers to and from it anywhere in the brainstem. Herein, we sought to determine the localizing value of INO plus ataxia in the rostrocaudal axis of the brainstem. Thirty patients with INO plus limb or truncal ataxia were subjected to analyses. For comparison, 20 patients with isolated INO without any ataxia served as the control. We determined the lesion extent in the MRIs responsible for INO plus ataxia using a probabilistic lesion mapping and subtraction analysis and analyzed the neuro-otologic findings using video-oculography. In patients with INO with limb or truncal ataxia, the responsible lesions were mostly restricted to the paramedian tegmentum at the pontomesencephalic junction. In contrast, the lesions causing isolated INO without ataxia were mostly located in the caudal or mid-pontine area. The rostro-caudal distribution of the lesions was similar among the patients with only limb ataxia (n=3), both limb and truncal ataxia (n=10), and only truncal ataxia (n=17). INO plus ataxia indicates a lesion involving the MLF at the pontomesencephalic junction. Damage to the brachium conjunctivum or mesencephalic locomotor region may explain the ataxia in association with INO in lesions involving this area.

ROSTRAL MIDBRAIN INFARCTION PRODUCING ISOLATED LATEROPULSION

A distinct syndrome characterized by lateropulsion arises from lacunar infarctions of the paramedian tegmentum of the rostral midbrain. Only a few reports are available, and in little more than a handful was the infarct documented with modern imaging techniques. We describe two cases and review the pertinent literature. ### Case reports. #### Patient 1. Over the course of 2 months, a 76-year-old man had several small vessel infarctions in various vascular territories. He had been anticoagulated with warfarin for chronic atrial fibrillation but his International Normalized Ratio was subtherapeutic during his first two hospitalizations for these events. He recovered without neurologic deficit and was discharged after warfarin adjustment and initiation of acetylsalicylic acid. He returned to the hospital 2 weeks later complaining of imbalance. On admission, his blood pressure was 161/74 mm Hg and his heartbeat was irregular at a rate of 78/minute. He was afebrile. Signs of meningeal irritation were absent. He was alert and oriented with fluent language. There were no abnormalities of conjugate gaze or pupil function, cyclotropia or head tilt. Gait and stance were wide based. There was lateropulsion to the left, both sitting and standing. MRI findings are shown in the figure. Duplex ultrasonography of neck vessels and echocardiography were unrevealing. After reversal of anticoagulation, a lumbar puncture was performed (protein 128 mg/dL, glucose 40 mg/dL …

Body lateropulsion as an isolated or predominant symptom of a pontine infarction

Background: Lateropulsion of the body—that is, falling to one side—is a well-known clinical feature of stroke in the posterior circulation. Body lateropulsion as an isolated or predominant manifestation of a...

Dissociation of hippocampal serotonin release and locomotor activity following pharmacological manipulations of the median raphe nucleus

In vivo microdialysis was used to investigate the role of serotonin in the locomotor hyperactivity produced by injections of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OHDPAT), muscimol and baclofen into the median raphe nucleus (MR) of unanesthetized rats. Intra-MR injections of the GABA A agonist muscimol (25 ng) resulted in a pronounced increase in locomotor activity which was accompanied by a 42% decrease in hippocampal serotonin release during the first hour following injection. Intra-MR injections of the GABA B agonist baclofen (125 ng) induced hyperactivity of a similar magnitude, but failed to affect hippocampal serotonin release. In contrast, the serotonin (5-HT 1A) agonist 8-OHDPAT (5 μg) produced only a small effect on locomotor activity but reduced hippocampal serotonin output by 51%. These findings demonstrate that it is possible to dissociate the effects of intra-MR drug injections on locomotor activity and hippocampal 5-HT release and strongly support the view that nonserotonergic neurons in the paramedian tegmentum are importantly involved in the control of behavioral arousal.

Crossed innervation of the superior rectus

We studied two patients which showed a paralysis of the oculomotor nerve on one side and isolated paralysis of the superior rectus on the other side. On the side of oculomotor nerve paralysis, midbrain infarct extending from the paramedian tegmentum to crus cerebri was demonstrated in one case who showed no recovery, and a small lacuna in midbrain tegmentum in another one who showed complete recovery. On the side of isolated paralysis of the superior rectus, no lesion was demonstrated by CT and MRI, and no clinical signs of the involvement of fiber tracts or nuclei were evident in both cases. A unilateral lesion of oculomotor nerve nucleus caused a paralysis of the contralateral superior rectus.

Comparative studies of locomotor behavior following microinjections of muscimol into various sites in the paramedian tegmentum

Microinjections of various doses of muscimol into the median raphe nucleus, the dorsal raphe nucleus or the caudal portion of the ventral tegmental area elicited dose-dependent increases in locomotor activity. In contrast, injections into the rostral portion of the ventral tegmental area or the midline pontine tegmentum caudal to the median raphe were ineffective. Lower doses of muscimol were required to produce hyperactivity after injections into the median raphe than after injections into any of the other sites. These findings suggest that the median raphe nucleus is the most sensitive site in the paramedian tegmentum for the elicitation of hyperactivity by muscimol.

Successful Evacuation of a Pontine Hematoma in Chronic Stage

A 52-year-old male was brought to Wakakusa Daiichi Hospital by ambulance because he had fallen unconscious. On admission he was stuporous. Neurological examination revealed left-sided facial palsy, left-sided ptosis, right-sided hemiplegia, and marked impairment of horizontal eye movement except for convergence. Computed tomography (CT) revealed a small high density area in the paramedian tegmentum. Cerebral angiography showed no abnormal vessels. Three hours after admission he became alert. One month after admission the right-sided hemiplegia improved, but he could not walk by himself. CT performed 45 days after admission showed a low density area in the pontine tegmentum with the fourth ventricle compressed persistently. Fifty days after admission, suboccipital craniectomy and evacuation of the hematoma was performed. The postoperative course was uneventful. One week after surgery the bulbar palsy improved and the tracheotomy could be closed. One month later, facial palsy and hemiplegia had so improved that he could close his eyes and walk without aids. Half a year after evacuation of the hematoma, the patient recovered to partially assisted daily life. Cases of primary pontine hemorrhage successfully evacuated have been reported, but the majority of primary pontine hemorrhages are treated conservatively. The importance of evacuation of primary pontine hemorrhage in the chronic stage was recognized.

Sources of direct excitatory and inhibitory inputs from the medial rhombencephalic tegmentum to lateral and medial rectus motoneurons in the cat.

The paramedian pontine and bulbar tegmentum was explored by microstimulation to outline the sites of origin of direct excitatory and inhibitory inputs to lateral rectus (LR) and medial rectus (MR) motoneurons (MNs). In order to avoid activation of fibers of passage and axon reflexes originating outside the stimulation sites, experiments were carried out 4--22 days after brain stem transections causing degeneration of vestibulo-ocular pathways. Additionally, in some experiments the paramedian tegmentum was isolated from the contralateral side by midline transections. Mapping of stimulus sites from which monosynaptic EPSPs and IPSPs were elicited brought out the following preoculomotor reticular regions: 1. LR-MNs received monosynaptic IPSPs from the contralateral reticular formation corresponding to Nucl. reticularis points caudalis (R.p.c.) and the rostral part of Nucl. reticularis gigantocellularis (R.gc.). 2. Monosynaptic inhibitory input to MR-MNs could only be demonstrated after degeneration of excitatory pathways ascending from the internuclear neurons of the VIth nucleus and from the ipsilateral vestibular nuclei. Monosynaptic IPSPs originated in the ipsilateral dorso-medial tegmentum through the entire extent of the Nucl. reticularis pontis oralis and rostral R.p.c. including the region of the ipsilateral VIth nucleus. 3. Monosynaptic excitation of LR-MNs was induced by stimulation of the ipsilateral R.p.c. and the rostral half of the paramedian bulbar tegmentum (R.gc.). 4. The sites from which monosynaptic EPSPs were evoked in MR-MNs were confined to the contralateral VIth nucleus and its immediate vicinity. No evidence could be obtained for direct excitatory inputs to MR-MNs from the ipsilateral paramedian tegmentum. It is concluded that the paramedian rhombencephalic reticular formation contains four pools of premotor neurons related to coordination of conjugate horizontal eye movements. Two of them are excitatory for LR- and MR-MNs with ipsilateral ON-directions, the other two mediate reciprocal inhibition of the antagonistic motor nuclei.