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We present the case of a young male with severe head injury, cervico-thoracic fractures, and an initially unrecognized brainstem infarct due to unilateral dissection of vertebral artery, who made an unusually excellent recovery. This report stresses the importance of prompt clinico-imaging diagnosis and prophylactic anticoagulant treatment in such cases.
A 60-year-old man with a 4-year history of intractable neck pain and radicular pain in the C5 nerve root distribution presented to our department for a CT-guided transforaminal left C5 nerve root block. He had had a similar procedure on the right 2 months previously, and had significant improvement of his symptoms with considerable pain relief. On this occasion he was again accepted for the procedure after the risks and potential complications had been explained. Under CT guidance, a 25G spinal needle was introduced and after confirmation of the position of the needle, steroid was injected. Immediately the patient became unresponsive, and later developed a MR-proven infarct affecting the left vertebral artery (VA) territory. This is the first report of a major complication of a cervical root injection under CT guidance reported in the literature. We present this case report and the literature review of the potential complications of this procedure.
We report the case of a patient with bilateral and symmetrical T2 hyperintensities of the middle cerebellar peduncles. She had a history of left pontine infarction 8 months before. This was attributed to bilateral Wallerian degeneration. MR Spectroscopy showed decreased N-acetyl aspartate/Creatine (NAA/Cr) ratio in the cerebellar peduncles as well as in the whole cerebellum. We hypothesize that this could reflect neuronal degeneration following a stroke.
OBJECTIVE: To describe the clinical features, MRI findings, and pathogenesis of strokes producing internuclear ophthalmoplegia (INO) as an isolated or predominant clinical manifestation. METHODS: Thirty patients presenting with INO without (n = 12) or with (n = 18) minimal other neurologic signs were studied. MRI and angiogram (conventional in 3, MR angiogram in 27) studies were performed in all of them. RESULTS: Twenty-four presented with INO, whereas six initially presented with one-and-a-half syndrome that changed into INO. Dorsal brainstem infarcts responsible for the INO were located in the caudal pons in 4, rostral pons in 8, rostral pons and isthmus in 2, isthmus area in 14, isthmus and midbrain in 1, and midbrain in 1 patient. Vascular lesions were found in the posterior circulation in 14 patients (47%): at the basilar artery (BA) in 4, superior cerebellar artery (SCA) in 4, posterior cerebral artery (PCA) in 4, and both the PCA and the SCA in 1. The INO eventually disappeared in all patients, tending to last longer (p = 0.05) when it was associated with other neurologic signs. CONCLUSIONS: Isolated or predominant INO is a unique clinical stroke syndrome caused by small dorsal brainstem infarction. The pathogenesis, however, is heterogeneous, including distal occlusion of small penetrating arteries, atheromatous branch occlusion from the BA, SCA, or PCA, or major BA occlusion. The functional prognosis of these patients is excellent, although the INO tends to last longer when there are other neurologic deficits.
The megadolichobasilar artery is a rare vascular disease, which usually becomes apparent either due to cerebral ischemia or due to compression of the brainstem or the cranial nerves, thereby leading to a large variety of neurological symptoms. We report on a patient who suffered a sudden right-sided deafness accompanied by vertigo and vomiting. Initially, an idiopathic sensorineural hearing loss was diagnosed and later on, after no improvement took place in spite of conservative therapy, a rupture of the round window membrane was suspected. Two weeks after the first symptoms had occurred the patient developed a hemiparesis on the left side.Radiology disclosed a dilated and partially thrombosed basilar artery as well as a paramedian pontine infarction. We therefore assumed that the patient's symptoms had been caused by thrombotic occlusion of the labyrinthine artery and several rami ad pontem. The article reviews the great variety of clinical symptoms caused by megadolichobasilar artery and discusses important therapeutic options.
The authors describe 2 cases of posterior fosa venous infarction. A 56-year-old woman with essential thrombocytemia presented with fluctuating complaints of headache, nausea, vomiting, left-sided numbness-weakness, and dizziness and became progressively stuporous. Cranial magnetic resonance imaging (MRI) showed bilateral parasagittal fronto-parietal and left cerebellar contrast-enhancing hemorrhagic lesions. On magnetic resonance venography, the left transverse and sigmoid sinuses were occluded. The second patient, a 39-year-old woman, presented with acute onset of diplopia, numbness of the tongue, vertigo, and right-sided weakness following a gestational age stillbirth. MRI revealed lesions in the right half of midbrain and pons and in the superior part of the right cerebellar hemisphere. Digital subtraction angiography showed right transverse and sigmoid sinus occlusion. The authors suggest that one should investigate the possibility of venous infarction in the presence of posterior fossa lesions that are often hemorrhagic and are not within any arterial territory distribution but respect a known venous drainage pattern. Recognition of the observed clinical and neuroimaging features can lead to earlier diagnosis and, potentially, more effective management.
A 21 year old woman presented with coma and quadriparesis secondary to bilateral pontine infarction. Three weeks later motor aprosodia was the most notable neurological finding apart from mild asymmetric limb weakness. No other supratentorial lesion was noted on initial and subsequent multimodality magnetic resonance imaging and magnetic resonance perfusion imaging revealed right frontotemporal hypoperfusion. This is the first report of aprosodia with an isolated brainstem lesion.
A patient with unilateral upper medial medullary infarction presented with contralateral paralysis of the pharyngeal constrictor muscle in association with lemniscal sensory loss, pyramidal insufficiency, and central facial palsy on the same side. Individual differences in supranuclear control of the pharyngeal muscles may explain this rare occurrence. The combination of these signs is described as a syndrome of upper medial medullary lesion.
We report a patient with medial medullary infarction who could be diagnosed in an early stage, and we discuss the role of diffusion-weighted magnetic resonance imaging (MRI) for stroke rehabilitation. In the case of our patient, the infarction was difficult to diagnose because the patient had atypical features and a past history of head injury. Nonetheless, we could diagnose the medial medullary infarction easily using diffusion MRI within several hours of onset. Then, a rehabilitation program was started the day after onset. We believe that diffusion MRI can be used as a useful method for very early stage diagnosis and to execute rehabilitation for early stroke patients.
BACKGROUND: Vertebrobasilar territory infarction is one of the rarer presentations of CVJ anomalies. A new radiologic sign due to stretching of the short third segment of VA detected on MRA/DSA may identify patients of AAD at risk of developing VBI. METHODS: Seven patients who presented with VBI were found to have a coexisting mobile (n = 6) or fixed (n = 1) AAD. None of these patients had the presence of any of the known risk factors for cerebrovascular disease. On identification of VBI on CT/MRI, DSA (n = 7) and MRA (n = 1) were performed to assess bilateral vertebral arteries. The course of normal VA was also studied in 5 control patients without AAD or VBI. RESULTS: Digital subtraction angiography/MRA showed obstruction of VA at the C1 through C2 level on one side in each of these cases. The third segment of the contralateral VA showed a shortened and straighter loop termed as the stretched loop sign of the VA. On DSA, the latter manifested as (a) opening of the distal loop of the VA as it emerges from the foramen transversarium of the atlas and traverses on the dorsum of the posterior arch of atlas (n = 3), (b) shortened and stretched VA that runs laterally and posteriorly forming the proximal loop after emerging from the foramen transversarium of the axis (n = 2), or (c) both (n = 2). All patients presented with the clinical manifestations of VBI. Only 2 of these had preexisting myelopathy and long tract signs conventionally attributable to AAD. CONCLUSION: Vertebrobasilar territory infarction in AAD may occur because of the obstruction of the third segment of VA. A shorter and straighter loop of the third segment of VA coexisting with an abnormal translational mobility between the atlas and the axis may be the etiopathogenetic factor.
BACKGROUND: Infarcts of the rostral brainstem often cause vertical gaze palsies but may also produce inappropriate convergence that manifests as pseudoabducens palsy and convergence-retraction nystagmus (CRN). Although the substrate for vergence has been defined in the monkey as lying dorsal and lateral to the oculomotor nucleus, the human homologue is unknown. METHOD: - The authors reviewed the clinical features, ocular findings, and CT or MR lesions in seven patients with pseudoabducens palsy and "top-of-the-basilar" infarction. They reviewed the literature for infarcts causing pseudoabducens palsy or CRN with precise autopsy localization. The authors then mapped the location of the infarcts on anatomic templates. RESULTS: The smallest MR infarct produced an ipsilateral pseudoabducens palsy and CRN, and was located just rostral to the oculomotor nucleus, near the midbrain-diencephalic junction. Two patients with only contralateral pseudoabducens palsy had both subthalamic and thalamic infarction. Four patients with bilateral pseudoabducens palsy had larger infarcts involving the midbrain. All patients with pseudoabducens palsy had upgaze palsy. Two patients with CRN from the literature had small infarcts near the midbrain-diencephalic junction at autopsy. CONCLUSIONS: Lesions near the midbrain-diencephalic junction are important for the development of pseudoabducens palsy. Pseudoabducens palsy and CRN are probably both manifestations of abnormal vergence activity. Inhibitory descending pathways for convergence may pass through the thalamus and decussate in the subthalamic region.
BACKGROUND AND PURPOSE: Vasculitis and infarcts are well-established sequelae of bacterial meningitis. However, early large-vessel involvement is rare, particularly within the brainstem. There has been one previous case report of a young male who presented with pontine infarct as an early manifestation of Streptococcus milleri meningitis. We present another case of brainstem infarction associated with meningitis caused by Streptococcus anginosus. CASE DESCRIPTION: We report a 58-year-old man who developed constitutional symptoms and gait instability, followed by progressive stupor. On examination, he had a Glasgow Coma Scale of 8 with intact brainstem reflexes and no focal findings. Magnetic resonance imaging documented bilateral pontine infarcts. S. anginosus was isolated from cerebrospinal fluid. Despite proper antibiotic treatment, the patient remained comatose and care was withdrawn. Postmortem examination revealed the meningitis was predominantly localized at the base of the brain. In addition, ventriculitis, multiple abscesses, and multiple infarcts in the pons and midbrain were found. CONCLUSION: S. anginosus, which is part of the normal human flora, causes invasive pyogenic infections and is an uncommon cause of bacterial meningitis. This type of infection is mostly situated at the base of the brain and has a propensity to encase the basilar artery and its perforators, thus causing brainstem stroke early in its course.
MRI including diffusion-weighted sequences (DW-MRI) has demonstrated its high sensitivity for acute supratentorial ischemic lesions. In this study we examined the sensitivity of different MRI sequences for the detection of acute brainstem and isolated thalamic infarctions. Diffusion- and T2-weighted MRI of 45 consecutive patients with signs and symptoms of infratentorial and thalamic infarction between 6/1997 and 1/2000 were analysed. The time between the onset of symptoms and the first MRI varied between 2 hours to 7 days with a median of 2 days. MRI repeats were performed in 4 patients in whom the clinical brainstem infarction had not been detected initially. Lesion detectability and size were evaluated for different brainstem and thalamic localizations. An acute brainstem or thalamic infarction as defined by the clinical condition could be identified in all patients by comparison of DW-MRI and T2-weighted images. Pons in farctions were the largest, followed by midbrain and thalamic lesions. Medulla oblongata infarctions were small in comparison. Pons, mid-brain and thalamic infarctions were reliably identified beginning 12 hours after the onset of symptoms. In contrast, detectability of medulla oblongata infarctions varied within the first 24 hours and their overall visibility was worse than that of other brainstem infarctions corresponding to their small size. However, regardless of loca tion, none of the 3 infarctions examined within the first 5 hours after the onset of symptoms could be identified. These lesions were demonstrated in follow-up examinations. In conclusion, pontine, midbrain and thalamic infarctions can reliably be visualized by a combination of DW-MRI and T2-weighted images beginning 12 hours after the ischemic attack. However, sensitivity seems to be lower earlier than 12 hours after ischemia and for medulla oblongata lesions.
We report the case of a 64-year-old man with sudden onset of numbness in the right hand and foot. Neurological examinations were normal except for hypersthesia, and hyperalgesia of the right hand and foot. Brain MRI demonstrated a high signal intensity on T2-weighted image and a low signal intensity on T1-weighted image in the left tegmetum of the pons. He was diagnosed with pontine infarction presenting with cheiro-pedal syndrome (CPS). Damage in the sensory pathways can cause CPS. Difference in the threshold may explain the specific sensory pattern in this syndrome. Further examination of the relationship between sensory symptoms and localization on MRI is needed to clarify this syndrome.
We reported a sixty-year-old man who developed acquired stuttering after a brainstem infarction. Infarctions were detected in the midbrain and upper pons. Neurogenic stuttering of this patients indicated that the midbrain and upper pons could be lesion sites responsible for acquired stuttering. We speculated that the reticular network extending from the brainstem to the frontal cortices, and the periaqueductal gray matter could be closely related regions generating neurogenic stuttering.
PURPOSE: To determine the feasibility and safety of stenting intracranial atherosclerotic stenoses. METHODS: In 12 patients the results of primary intracranial stenting were evaluated retrospectively. Patient ages ranged from 49 to 79 years (mean 64 years). Six patients presented with stenoses in the anterior circulation, and six had stenosis in the posterior circulation. One patient presented with extra- and intracranial tandem stenosis of the left internal carotid artery. Three patients presented with acute basilar thrombosis, caused by high-grade basilar stenoses. RESULTS: Intracranial stenoses were successfully stented in 11 of 12 patients. In one patient the stent could not be advanced over the carotid siphon to reach the stenosis of the ophthalmic internal carotid artery. Follow-up digital subtraction angiographic studies were obtained in two patients who had presented with new neurologic signs or symptoms. In both cases the angiogram did not show any relevant stenotic endothelial hyperplasia. In one patient, after local thrombolysis the stenosis turned out to be so narrow that balloon angioplasty had to be performed before stent deployment. All three patients treated for stenosis-related basilar thrombosis died due to brainstem infarction that had ensued before the intervention. CONCLUSIONS: Prophylactic primary stenting of intracranial stenoses of the anterior or posterior cerebral circulation can be performed with a low complication rate; technical problems such as stent flexibility must still be solved. Local thrombolysis followed by stenting in stenosis-related thrombotic occlusion is technically possible.
The one-and-a-half syndrome is characterised by a lateral gaze palsy in one direction and internuclear ophthalmoplegia in the other. It is due to a unilateral lesion of the dorsal pontine tegmentum, involving the ipsilateral paramedian pontine reticular formation, internuclear fibres of the ipsilateral medical longitudinal fasciculus and, usually, the abducens nucleus. The main causes of this rare syndrome are stroke and multiple sclerosis. Few cases have been reported since the introduction of MRI. Our aim was to examine clinicoradiological correlations in six patients with a one-and-a-half syndrome due to a stroke. Ophthalmological symptoms were diplopia, oscillopsia or blurred vision. Four patients had an associated facial nerve palsy, three a hemiparesis and one a unilateral hemihypoaesthesia. MRI revealed an infarct in the pons in all patients. The cause of the infarct was a basilar artery dissection in one patient, bilateral vertebral artery dissection in a second and unknown in the other four. All patients recovered within 2 days to 8 weeks. This study showed a good correlation between the site of the lesion (superior, inferior or extensive pontine ischaemia) and clinical deficits.
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.