Midbrain Stroke Research Articles

Isolated unilateral oculomotor paresis in pure midbrain stroke

Background and purposePure midbrain stroke can cause isolated unilateral oculomotor paresis. We attempted to determine whether there is a difference in the oculomotor paresis pattern between pure midbrain infarction and midbrain hemorrhage. MethodsPure midbrain stroke patients who presented with isolated unilateral oculomotor paresis were identified from a group of 2447 consecutive patients hospitalized for acute cerebral infarction or hemorrhage during the period May 2008 through April 2014. Detailed oculomotor findings were evaluated in the identified patients per the cause of the stroke. ResultsFive patients with infarct and 1 with hemorrhage became our study subjects. Lesions were located in the paramedian area of the midbrain involving the oculomotor fascicles. The pupillary sphincter and inferior rectus muscles were selectively spared in the infarct patients, whereas these muscles were selectively affected in the hemorrhage patient. ConclusionFibers in the oculomotor fascicle that innervate the levator palpebrae, superior rectus, and inferior oblique muscles appear to be more susceptible to ischemic damage than those that innervate the pupillary sphincter and inferior rectus muscles. Isolated impairment of the pupillary sphincter and inferior rectus muscles may be suggestive of a non-ischemic process.

Monocular Diplopia Associated with a Midbrain Stroke

Background and Purpose Monocular diplopia is often due to intraocular disease. It is rarely the result of cerebral causes, which include lesions in or near Brodmann’s area nineteen, the frontal eye fields or the cerebellum. Monocular diplopia has not been reported in a patient with a midbrain lesion. Methods and Results A patient with a history of hypertension presented with right monocular diplopia and headache. There was no ocular cause of the patient’s symptoms, and aside from bilateral ptosis, there were no relevant findings on neurological examination. MRI brain revealed an ischemic stroke affecting the right oculomotor nucleus. Her evaluation, including an ECG and 48-hour Holter monitor was unremarkable. A subsequent 30-day auto-trigger cardiac event monitor revealed paroxysmal atrial fibrillation. Conclusions This case shows that monocular diplopia can be associated with a midbrain lesion and underscores the importance of prolonged cardiac monitoring in patients with otherwise cryptogenic stroke.

Manifestations of stroke

The book is divided into two parts namely “Neurologic and Other Disorders” and “Topographic Syndromes”. The first section begins with the motor syndromes, the most common stroke clinical syndrome. The authors have elaborated the various motor manifestations in a simple way. The stroke sensory syndromes are dealt with in a concise manner. The chapter on eye movement abnormalities is very informative. However, inclusion of a few images showing the neuroanatomical pathway would have made it easy to understand. The chapter on visual dysfunctions deals with the visual symptoms in relation to the optic nerve pathway and also covers various visual phenomena. One of the important aspects of stroke clinical diagnosis is differentiating between anterior and posterior circulation strokes. The chapter on dizziness and vertigo explains the clinical clues in localising posterior circulation strokes in relation to the presence of dizziness and vertigo. The chapter “Impaired Consciousness”, covers the various types of disturbances in consciousness. Also, the coma like states which are important in the prediction of prognosis in stroke patients have been discussed. The chapter on language disorders in stroke is very simple and easy to understand. The common language dysfunctions in stroke are discussed well. The section on memory dysfunction is short and crisp. One of the intriguing aspects of stroke is right hemisphere syndromes. Although the symptomatologies of right hemisphere stroke have been enumerated, this section could have been organized better to improve readability. Vascular cognitive impairment (VCI) is an important post-stroke disability. Post-stroke dementia and cognitive impairment are covered well including the various criteria used for the diagnosis of VCI. One of the neglected disabilities is anxiety and depression after stroke. The chapter on mood disorders contains the risk factors for anxiety and depression after stroke. In addition, the authors have elaborated on the diagnosis and treatment of these conditions. Stroke disconnection syndromes such as apraxia, agnosia, etc, are described in detail. The common disconnection syndromes are also explained well. Autonomic dysfunctions in stroke are commonly seen. The salient autonomic syndromes that occur following stroke are highlighted along with explanation on the neuroanatomical correlates. Another common speech disorder which occurs in stroke is dysarthria/mutism which can vary according to the site of the lesion and this section also is well covered. The pathophysiology, diagnosis and treatment of post-stroke dysphagia are discussed in a comprehensive manner including the various tools used to evaluate dysphagia. Certain strokes can present with breathing difficulties. The physiology, pathophysiology and clinical syndromes of ventilatory disorders are dealt with methodically. The chapter on lacunar strokes describes the different types of lacunar syndromes and also focus on the pathogenesis and outcome in these patients. The second section of the book begins with a lucid chapter on arterial territories of the brain. Brain maps of various territories in the cerebrum, brainstem and cerebellum are included. The territories depict the neuroimaging sections in clinical practice. This section lays down the foundation for the remaining chapters of the book. All the chapters begin with basic anatomy, aetiology and then elaborate the clinical features. The chapters on thalamic, caudate and putaminal infarcts/haemorrhages are very informative. The pathophysiology of lobar haemorrhage including the mechanisms of raised intracranial tension is explained clearly. The chapter on subarachnoid and intraventricular haemorrhage gives an overview of the two important conditions. The large hemispheric infarction deals with the current concepts in pathophysiology and also about the recent surgical trials. There is some degree of repetition in the chapters on midbrain, pontine and medullary strokes. The presentations, aetiologies and prognosis of cerebellar strokes are appropriate. The strokes in the territories of vertebral, basilar and carotid arterial occlusions are described very well. Finally, the last last two chapters also discuss venous ischaemic and spinal cord syndromes. In the era of modern technology where less importance is given for bedside skills, this book will be a great asset to neurology residents, neurologists and stroke neurologists/physicians.

Acute Psychosis Associated with Subcortical Stroke: Comparison between Basal Ganglia and Mid-Brain Lesions.

Acute onset of psychosis in an older or elderly individual without history of previous psychiatric disorders should prompt a thorough workup for neurologic causes of psychiatric symptoms. This report compares and contrasts clinical features of new onset of psychotic symptoms between two patients, one with an acute basal ganglia hemorrhagic stroke and another with an acute mid-brain ischemic stroke. Delusions and hallucinations due to basal ganglia lesions are theorized to develop as a result of frontal lobe dysfunction causing impairment of reality checking pathways in the brain, while visual hallucinations due to mid-brain lesions are theorized to develop due to dysregulation of inhibitory control of the ponto-geniculate-occipital system. Psychotic symptoms occurring due to stroke demonstrate varied clinical characteristics that depend on the location of the stroke within the brain. Treatment with antipsychotic medications may provide symptomatic relief.

Acute Disseminated Encephalomyelitis Masquerading as Midbrain Stroke: A Case Report

Acute Disseminated Encephalomyelitis Masquerading as Midbrain Stroke: A Case Report

A Rare Case of Isolated Left Medial Midbrain Stroke

Midbrain stroke is uncommon. We are presenting an interesting case of a patient with rare isolated left midbrain stroke. The patient had third cranial nerve palsy. Magnetic resonance imaging (MRI) brain showed acute stroke at the medial part of left midbrain. Magnetic resonance angiography (MRA) was normal.

Pupil-sparing complete third nerve palsy from cryptogenic midbrain stroke in an otherwise-healthy young adult with patent foramen ovale

Although pupil-sparing in acute unilateral complete third nerve palsy is often a sign of ischemic nerve injury, it is not specific for injury outside of the midbrain. This report documents acute pupil-sparing complete third nerve palsy in an otherwise healthy young adult with patent foramen ovale and associated atrial dilatation who suffered cryptogenic focal midbrain stroke, presumably from a paradoxical embolism. The patent foramen ovale was surgically closed. Over the next several months neurological recovery was complete except for diplopia and relatively comitant hypotropia, which responded well to conventional strabismus surgery.

Life-threatening bradycardia after bilateral paramedian thalamic and midbrain infarction

Dear Sirs,Bilateral symmetric thalamic infarcts are uncommon pre-sentations of ischemic stroke that mostly occur in the ter-ritories of the paramedian thalamic arteries [1]. Thesearteries arise either separately from the posterior cerebralarteries (PCAs) or exceptionally from a single commontrunk the artery of Percheron [2]. In this article, a case ofbithalamic paramedian and midbrain stroke presenting withdrowsiness, ophtalmoplegia, and life-threatening brady-cardia is presented. Despite it is known that different stroketopographic patterns can produce slowing of heart rate andasystolia, this is the first report of acute bradycardia inconcomitance to bilateral midbrain infarction [3–5].A 51-year-old man with a 3-year history of idiopathicarterial hypertension (on zofenopril) was admitted to ouremergency room after being found unresponsive in bed. Onadmission he showed fluctuating level of consciousness,dysarthria, anisocoria, and vertical gaze palsy (NIHSS 7,GCS 9). During examination, the patient suddenly devel-oped severe sinus bradycardia (pulse rate \30 beats perminute (bpm), for 3 minutes) that improved only afteratropine administration. Arterial blood pressure (BP),blood exams, toxicological screening, and brain CT scanwere all normal. Within 1 h, another self-limiting episodeof drowsiness and concomitant bradycardia ensued. Dif-fusion-weighted (DW) sequences on brain MRI demon-strated symmetric bilateral thalamic, hypothalamic, andmidbrain acute infarctions, thus, advocating the occlusionof a putative artery of Percheron (Fig. 1a). Top-of-the-basilar syndrome was ruled out documenting patency ofthe basilar artery and both PCAs by MRI angiography.Extensive cardiological workup showed no signs ofhypertensive cardiomyopathy both on ECG and echocar-diography, but revealed a patent foramen ovale (PFO) withsevere right-to-left atrial shunt. Anticoagulant therapy was,therefore, started and PFO closure suggested. In the fol-lowing days, episodes of bradycardia (nadir of 38 bpm,without major alterations of BP) tended to recur duringdrowsiness and night sleep. Particularly, diurnal fluctua-tions of vigilance paralleled recurrent sleep spindle patternson electroencephalography (Fig. 1b). Sinus bradycardiaoccurred less often and heart rate gradually increased in thefollowing weeks. At the 3-month follow-up, despite fullresolution of gaze palsy and arrhythmia, the patient stillpresented recurring episodes of hypersomnolence andimportant disability due to long-lasting apathy.Infarcts at the mesencephalic–diencephalic junctionresult in complex clinical syndromes contingent on thedeep brain structures involved. Supranuclear vertical gazepalsy and associated abnormal ocular reflexes are related tolesions of the rostral interstitial and Edinger–Westphalnuclei [6]. Fluctuating level of consciousness, coma, andhypersomnolence are attributed to the involvement ofintralaminar nuclei and reticular mesencephalic formation[7]. Notably, while presenting symptoms usually reverseover time, cognitive dysfunctions caused by limbic loopinterruption lead to long-term disability [8]. In our patient

Third Nerve Palsy: Analysis of 1400 Personally-examined Inpatients

Most studies of third nerve palsy (TNP) antedate computerized imaging and focus primarily on chart review of referral outpatients. To compare a large contrasting population, I reviewed 1400 personally-examined municipal hospital inpatients with TNPs seen over 37 years. TNPs were bilateral in 11%, complete in 33%, without other neurological signs (isolated) in 36%, and associated with recurrent cranial neuropathies in 7%. Third nerve damage occurred in the subarachnoid space in 32%, the cavernous sinus in 23%, the brainstem in 14%, as a nonlocalized peripheral neuropathy in 18% and at an uncertain location in 13%. Causes were trauma (26%), tumor (12%), diabetes (11%), aneurysm (10%), surgery (10%), stroke (8%), infection (5%), Guillain-Barre and Fisher syndromes (5%), idiopathic cavernous sinusitis (3%), benign self-limited (2%), miscellaneous (4%), and unknown (3%). Local causes, besides an abundance of trauma, included six cases involving cysticercosis, four with wound botulism, and one with coccidiomycotic meningitis. Of 234 patients with diabetes, microvascular ischemia was the cause of TNP in only two-thirds (five had aneurysms) and 53% of those with diabetic microvascular ischemia had pupillary involvement-often bilateral, suggesting concomitant autonomic neuropathy. Only 2% of aneurysms spared the pupil. Apainful onset occurred with 94% of aneurysm and 69% of diabetic cases. Bilateral TNPs, multiple cranial neuropathies, and accompanying neurological signs were common among our inpatients, as were causes rare in outpatient settings such as severe trauma, transtentorial herniation, midbrain strokes, and the Guillain-Barre syndrome. Few cases remained undiagnosed and nondiabetic ischemia was rare.

Teaching Neuro Images : Holmes tremor after midbrain stroke

A 69-year-old man presented with a continuous right upper extremity resting tremor with a 3-Hz frequency (video on the Neurology ® Web site at www.neurology.org). The tremor developed gradually, 4 months after a left midbrain stroke. MRI showed an infarct in …

Isolated trochlear palsy due to midbrain stroke

Trochlear palsy from intra-axial lesions usually accompanies other neurological deficits, and isolated trochlear palsy due to midbrain stroke is extremely rare. We report two patients with isolated trochlear nerve palsy due to circumscribed dorsal midbrain strokes, one from infarction and the other from hemorrhage, which are located in the region of the trochlear nucleus or adjacent fascicle. Focal brain stem stroke should be considered as a rare cause of trochlear palsy even though there are no associated neurological deficits.

Animal models of action tremor.

This article is devoted to animal models of tremors that emerge from lesions in the Guillain-Mollaret triangle. Cerebellar intention tremor is caused by lesions in the brachium conjunctivum or in the interpositus nucleus, possibly in combination with damage to the dentate nucleus. Impaired feed-forward motor control delays the braking of rapid movements, resulting in target overshoot and subsequent oscillation. Transcortical and transcerebellar sensorimotor loops undergo oscillation at a frequency that depends on the mechanical properties of the limb and the length of the sensorimotor loop (mechanical reflex oscillation). The crescendo quality of intention tremor may be a result of amplification of tremor in reverberating brain stem-cerebellar or thalamocortical loops. So-called rubral or midbrain tremor is caused by a combination of damage to the brachium conjunctivum and nigrostriatal pathways in the vicinity of the red nucleus. Secondary compensatory changes in the motor system are probably involved because midbrain tremor in people usually begins weeks or months after a midbrain stroke or trauma. Harmaline causes enhanced neuronal synchrony and rhythmicity in the inferior olive; this animal model, although as yet unproven, is the most popular one for essential tremor (ET). Additional studies in laboratory animals are needed to define the seemingly universal involvement of the cerebellum and ventrolateral thalamus (ventralis intermedius [Vim]) in virtually all human tremor disorders.

Midbrain Stroke With Angiogram-Negative Subarachnoid Hemorrhage Mimicking a Perimesencephalic Bleed

Angiogram-negative atraumatic subarachnoid hemorrhage (SAH) in a perimesencephalic pattern on computed tomography (CT) is associated with an almost invariably favorable prognosis with few rebleeds. We report a patient who exhibited a perimesencephalic hemorrhage pattern on CT and negative serial angiograms and who presented with severe neurologic disability from a concurrent midbrain stroke. We contend that both the acute infarction and hemorrhage arose from obliteration of a penetrating end artery. Possible etiologies of angiogram-negative SAH, including perimesencephalic hemorrhage, are discussed.

Isolated fascicular oculomotor nerve palsy as the initial presentation of the antiphospholipid syndrome

This case report describes a 24-year-old female who presented with sudden onset of painless diplopia and ptosis in her left eye. Examination identified an isolated incomplete pupil-sparing left oculomotor nerve palsy. Magnetic resonance imaging demonstrated focal hyperintensity in the left midbrain with infarction suggested by diffusion-weighted imaging. A diagnosis of primary antiphospholipid syndrome was made with the demonstration of a positive lupus anticoagulant. Other autoimmune markers were present on initial assessment, but did not fulfil diagnostic criteria for systemic lupus erythematosus. Anticoagulation with warfarin was commenced, with gradual resolution of neurological deficits. This case illustrates an unusual initial manifestation of primary antiphospholipid syndrome causing midbrain stroke in a young woman.

Oculomotor synkinesis following a midbrain stroke

A 33-year-old man developed a complete third nerve palsy in the setting of acute bacterial endocarditis. MRI revealed an ischemic stroke in the cerebral peduncle involving the third nerve fascicle. Subsequently, he was observed to have paradoxic elevation of the eyelid on adduction and downgaze. To the authors' knowledge, this is the first demonstration of oculomotor synkinesis after an acquired, ischemic CNS lesion.

Bilateral convergence nystagmus in unilateral dorsal midbrain stroke due to occlusion of the superior cerebellar artery

The authors report a 33-year-old man with left dorsal pontomesencephalic and cerebellar infarction due to an angiographically verified left superior cerebellar artery (SCA)-occlusion. Clinical presentation included dysarthria, homolateral limb ataxia, gait ataxia and contralateral spinothalamic sensory loss. Additionally, skew deviation, bilateral convergence nystagmus and pseudo-sixth nerve palsy of the left eye were observed. Vertical gaze and pupillary light reactions were preserved.This observation expands the spectrum of eye movement abnormalities due to midbrain involvement in isolated SCA-stroke and confirms a mesencephalic tectal territory of irrigation supplied by this artery. Additionally, it might give further evidence for the hypothesis of premotor control of convergence at a higher than mesencephalic level.

The spectrum of vertical gaze palsy following unilateral brainstem stroke

A single unilateral lesion, near the midline, may interrupt the pathways involved in vertical gaze just before and after they decussate, inducing an anatomically unilateral, but functionally bilateral, lesion. We report 11 patients with supranuclear vertical gaze palsies (two with conjugate upgaze palsy, four with combined up- and downgaze palsies, two with monocular elevation palsy, and three with vertical "one-and-a-half" syndrome) due to unilateral midbrain strokes.

Fascicular third nerve palsy with decreased vertical saccade velocity of the contralateral eye

A 59-year-old patient with an ischemic right unilateral midbrain stroke is described who exhibited a complete right fascicular third nerve palsy and in addition a vertical gaze paresis. After six months the disturbance of the vertical gaze could be demonstrated by slow saccades of the contralateral left eye, whereas the right third nerve palsy had only moderately improved. The lesion in the medial part of the midbrain tegmentum could be well demonstrated on MRI. The authors conclude that vertical saccades may be selectively disturbed, leaving the range of the slow vertical eye movements intact; moreover, a unilateral midbrain lesion may be sufficient to disturb vertical gaze.