A case report of central respiratory failure due to hemimedullary syndrome]

A hemimedullary infarction, in which both medial and lateral medullary infarctions occur simultaneously, is a rare cerebrovascular disease. Pontomedullary lesions often cause central respiratory failure, and the majority of central respiratory failures are due to bilateral pontomedullary lesions. We report a 66-year-old man with central respiratory failure due to a hemimedullary infarction detected by magnetic resonance imaging. He was admitted to our hospital on March 7, 1998, because of a sudden onset of dysarthria, and both numbness and weakness on his left side. Soon after arriving at the hospital, his spontaneous respiration ceased. Therefore, he was intubated and artificial ventilation was started. Pertinent neurological abnormalities on admission consisted of dysarthria, dysphagia, right Horner's sign, right gaze evoked horizontal nystagmus, right soft palate palsy, and tongue deviation to the right. In addition, left hemiparesis, left Babinski's sign, sensory impairment on the left side including the face, and central respiratory failure were noted. Although voluntary respiration recovered in 12 days, sleep apnea continued for 5 months, which was considered to be due to the automatic respiratory failure. An important feature of this patient was that the hemimedullary infarction caused the central respiratory failure. To our knowledge, this is the third patient whose central respiratory failure occurred because of a hemimedullary infarction.     

Bilateral medial medullary infarction due to bilateral vertebral artery dissection

We describe a 52-year-old woman who experienced transient motor weakness and numbness of the left extremities and presented 2 days later with severe hemiparesis and sensory impairment of the right extremities and right lingual palsy. Magnetic resonance imaging (MRI) revealed bilateral upper medial medullary infarction, primarily in the left ventral portion. The findings of both three-dimensional (3D) computed tomographic and conventional angiography suggested dissection of both intracranial vertebral arteries (VAs). Medial medullary infarction is generally caused by atherosclerosis within a VA or anterior spinal artery. This is the first report of bilateral medial medullary infarction due to dissection of both intracranial VAs.     

A case of bilateral cerebellar infarction in the distribution of the bilateral superior cerebellar artery]

We reported a case of bilateral cerebellar hemorrhagic infarction in the distribution of the bilateral superior cerebellar artery. A 58-year-old man suddenly developed dizziness and transient loss of consciousness. The neurological examination revealed left hearing disturbance, left sensory disturbance involving face, dysarthria and bilateral ataxia. This patient was considered to be classic clinical syndrome of right superior cerebellar artery. CT and MRI revealed hemorrhagic infarction corresponding to the full territory of the bilateral superior cerebellar artery. The right posterior cerebral artery was filling through the right posterior communicating artery on the right carotid angiography taken 2 hours after the onset. Bilateral vertebral angiography on the 18th day demonstrated no occlusions in the basilar artery and the bilateral superior cerebellar artery. Hemorrhagic infarction corresponding to the full territory of the bilateral superior cerebellar artery, sparing other territories as the present case, is extremely rare. In this case, cerebral embolism (top of the basilar syndrome) was suggested because of existence of atrial fibrillation and sudden onset.     

Persistent primitive first cervical intersegmental artery (proatlantal artery II) with occlusion of the basilar artery--a case report

A rare case of persistent primitive first cervical intersegmental artery (proatlantal artery II) is reported. A 58-year-old man was admitted to our hospital with dysarthria and left hemiparesis. On admission he was stuporous with bilateral gaze palsy and left hemiparesis. CT scan on admission showed low density areas in the right cerebellar hemisphere and ventricular part of the pons. Right retrograde brachiography revealed occlusion of the basilar artery, aplasia of the right vertebral artery and an abnormal vessel connecting the right external carotid artery and the right vertebral artery. This anastomotic vessel was thought to be a persistent primitive first cervical intersegmental artery (Proatlantal artery II). Left carotid angiography revealed the left posterior cerebral artery was visualized through the posterior communicating artery, leading from the internal carotid artery. Left retrograde brachial angiography showed that the left vertebral artery terminated just distal from the branching of the left posterior inferior cerebellar artery. After admission the left hemiparesis deteriorated gradually and tracheotomy was done due to respiratory difficulties. The patient was then transferred to the rehabilitation center on his 34th day in hospital with neurological deficits.     

Bilateral cerebral hemispheric infarction associated with sildenafil citrate (Viagra®) use

Sildenafil citrate (Viagra^®) is one of the frequently prescribed drugs for men with erectile dysfunction. We describe a 52-year-old man with bilateral middle cerebral artery (MCA) territory infarction after sildenafil use. He ingested 100 mg of sildenafil and about 1 h later, he complained of chest discomfort, palpitation and dizziness followed by mental obtundation, global aphasia and left hemiparesis. Brain magnetic resonance imaging documented acute bilateral hemispheric infarction, and cerebral angiography showed occluded bilateral MCA. Despite significant bilateral MCA stenosis and cerebral infarction, systemic hypotension persisted for a day. We presume that cerebral infarction was caused by cardioembolism with sildenafil use.     

A case of cerebral thrombosis presenting global aphasia without hemiparesis]

We reported a 62-year-old male with cerebral thrombosis presenting global aphasia without hemiparesis. The patient had an episode of aphasia 15 years ago, but recovered within 6 months. This time he had transient right sided mild hemiparesis, then he became aphasia next morning. When we examined at day 10 and day 15, his consciousness was clear, nothing he could speech, he could not understand or repeat. We diagnosed him global aphasia, but he had no hemiparesis except for right facial mild paresis and was able to walk. CT scan showed low density area in left and right posterior, left anterior watershed and left terminal zone. Cerebral angiography disclosed thrombotic occlusion of main trunk of left middle cerebral artery, and ambient segment of right posterior cerebral artery. Global aphasia without hemiparesis has been said a sign of embolic encephalopathy. This case was considered a very rare case, because he revealed global aphasia without hemiparesis by thrombotic occlusion.     

A case report of bilateral cerebral peduncular infarction manifesting tetraparesis and pseudobalbur palsy]

A 63-year-old female had presented with right hemiparesis and slight dysarthria. MRI had showed the infarction of left pons and left peduncle. Three months later she further presented with left hemiparesis, severe dysarthria and swallowing disturbance. MRI showed bilateral cerebral peduncular infarction. And the angiogram showed the occlusion of basilar artery at the just distal portion of the superior cerebellar artery. We recognized our case as the infarction due to the basilar artery occlusion. The 16 cases of bilateral cerebral peduncular infarction were reported. In these reports, the symptoms of bilateral cerebral peduncular infarction were locked-in syndrome in 15 cases and persistent vegetative state in only one case. Our patient presented with tetraparesis and pseudobalbur palsy not with locked-in syndrome, probably because the area of infarction was limited within almost lateral portion of peduncle. The sparing of posterior cerebral artery was one of the reason of such a condition. This is the first report of bilateral cerebral peduncular infarction manifesting tetraparesis and pseudobalbur palsy.     

Intracerebral and subarachnoid hemorrhages after administration of recombinant tissue plasminogen activator in a patient with acute ischemicstroke due to anterior cerebral artery dissection: a case report

A 45-year-old man was admitted to our hospital for treatment of right hemiparesis. At admission, he was alert and well oriented. His verbal comprehension seemed good, but his speech was not fluent. He could not stand or walk owing to the right hemiparesis, which was severe in the lower extremity. Computed tomographic (CT) scans on admission showed no abnormality. Diffusion weighted magnetic resonance imaging performed after the CT showed a high-intensity lesion in the left cingulate gyrus. Magnetic resonance angiography (MRA) revealed occlusion and irregularity of the left A2 portion of the anterior cerebral artery (ACA). At 1 h 50 min after the onset of the hemiparesis, recombinant tissue plasminogen activator (rt-PA; 0.6 mg/kg) was administered intravenously. At 1 h after the administration of rt-PA, he became drowsy and his right hemiparesis deteriorated. CT scans performed again showed a hematoma in the left frontal lobe and subarachnoid hemorrhage in the anterior interhemispheric fissure. He was treated conservatively. MRA performed on the 18th day after admission showed recanalization of the left ACA and abnormal dilatation of the left A2 segment. The abnormal dilatation was also depicted by 3D-CT angiography (3D-CTA) performed on the 26th day after admission and even on the 33rd and 77th days. As seen in our case, the definite diagnosis of dissection confined to the ACA frequently needs serial angiographies; therefore, its diagnosis immediately after the onset is often difficult. Thrombolytic therapy by intravenous administration of rt-PA for cerebral infarction caused by dissection of the ACA may recanalize the occluded site and facilitate the progression of the dissection, resulting in intracerebral and/or subarachnoid hemorrhages. In patients with cerebral infarction due to ACA dissection, strict control of blood pressure and careful observation are necessary after thrombolytic therapy by rt-PA.     

A case of acute cervical epidural hematoma mimicking medial medullary infarction complicated by arterial dissection]

A 67-year woman with hypertension rapidly noted weakness of the right upper and lower extremities with posterior cervical pain. At admission to our hospital, she showed right hemiparesis without facial palsy, and bilateral pathological reflex. Chest X-ray demonstrated enlargement of the mediastinal shadow. We suspected that she developed aortic arch dissection extending into the vertebral arteries and subsequent medial medullary infarction. However, enhanced thoracic CT, brain MRI-DWI and MRA examinations were negative. Her symptoms rapidly recovered three hours after the onset. A cervical MRI study revealed cervical epidural hematoma locating between the C3 and C6, which suppressed right side of the spinal cord. In conclusion, cervical epidural hematoma as well as medial medullary infarction complicated by the vertebral arterial dissection should be urgently explored when a patient had a sudden onset of cervical pain and hemiparesis without facial palsy.     

A case of medullary infarction presented lateral medullary syndrome and respiratory arrest after ataxic respiration

We reported a 71-year-old male with lateral medullary syndrome presented acute respiratory arrest after ataxic respiration. The patient had experienced transient diplopia repeatedly for about 2 weeks and then the developed persistent diplopia and vertigo. On the third day he was admitted to our hospital because of neurological deterioration and aspiration pneumonia. He showed left Horner's sign and double vision. And he had sensory disturbances of pain and temperature in the left face and the right side of the body, left limb ataxia and truncal ataxia. He showed dysarthria, severe dysphagia and left mild central facial paresis, but no hemiparesis. This case was clinically considered to be a typical case of left lateral medullary syndrome. When he was admitted to our hospital, he showed hypoxia with hypercapnea in spite of no history of chronic obstructive pulmonary disease. This condition was considered to be a central alveolar hypoventilation. He had two episodes of sudden-onset respiratory arrest following ataxic respiration on the 4th and 5th days, but no cardiac arrest. He was supported his respiration by mechanical ventilation until he was able to breathe spontaneously on the 29th day. The 22nd day MRI disclosed high intensity area in the left lateral and dorso-medial medulla in T2-weighted image, and this lesion was 1.5 cm in length. Therefore this case was diagnosed medullary infarction. This case developed ipsilateral facial pain in chronic stage. Pain existed around the eye and in the cheek, and pain was like toothache and unbearable like thalamic pain.(ABSTRACT TRUNCATED AT 250 WORDS)     

Lateral medullary infarction with ipsilateral hemiparesis,lemniscal sensation loss and hypoglossal nerve palsy

Here, we present a rare case of a lateral medullary infarction with ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy. In this case, we proved Opalski’s hypothesis by diffusion tensor tractography that ipsilateral hemiparesis in a medullary infarction is due to the involvement of the decussated corticospinal tract. We found that the clinical triad of ipsilateral hemiparesis, lemniscal sensation loss and hypoglossal nerve palsy, which had been regarded as a variant of medial medullary syndrome, turned out to be caused by lateral lower medullary infarction. Therefore, this clinical triad does not imply the involvement of the anteromedial part of medulla oblongata, when it is hard to distinguish a massive lateral medullary infarction from a hemimedullary infarction merely from MR images. At last, we suggest that hyperreflexia and Babinski’s sign may not be indispensable to the diagnosis of Opalski’s syndrome and we propose that “hemimedullary infarction with ipsilateral hemiparesis” is intrinsically a variant of lateral medullary infarction.     

Systemic lupus erythematosus manifesting as subarachnoid hemorrhage induced by cortical venous thrombosis and followed by medial medullary infarction]

A 43-year-old female, who had been treated for systemic lupus erythematosus (SLE), presented with a subarachnoid hemorrhage (SAH) induced by rupture of cortical venous thrombosis, and be followed by medial medullary infarction during the acute stage of the SAH. The patient initially manifested a SAH. Angiography demonstrated no evidence of any aneurysms or arteriovenous malformations, but revealed cortical venous thrombosis. She suddenly developed left hemiplegia caused by medial medullary infarction on the 6th day. An active anticoagulant therapy was thought to be inappropriate because of initial symptoms as a hemorrhage. Since she had been accompanied by the medullary infarction, then, initially started by antiplatelet therapy. After the confirmation of no saccular or dissecting aneurysms with 2nd angiography, her treatment could be changed to anticoagulant therapy. Because of the sustained negative reactions of anti-cardiolipin beta 2 glycoprotein I antibody and lupus anticoagulant during the course of SLE, the definite diagnosis of antiphospholipid syndrome (APS) could not be made. However, this case is pathogenically thought to be cerebrovascular disease based upon APS, considering that this syndrome may be related to various antigen/antibody systems.     

Bilateral medial medullary infarction presenting as vertical gaze palsy]

A 79-year old man noticed paresthesia in all 4 limbs, quadriplegia and dysarthria, and then developed respiratory arrest requiring mechanical ventilation. After level of consciousness was improved, vertical gaze palsy, left hemifacial palsy (central type) and quadriplegia were noted. Brain magnetic resonance imaging (MRI) on day 9 revealed bilateral upper medial medullary infarction. In general, the vertical gaze center is thought to be present in the midbrain, including the rostral interstitial nucleus of the medial longitudinal fasciculus, posterior commissure and interstitial nucleus of Cajal. Few reports have described vertical gaze palsy due to medullary lesions. The upper medial medullary lesions, particularly the paramedian tract in the medulla, may have been responsible for vertical gaze palsy in this patient.     

Recurrence of bilateral spontaneous cervical internal carotid artery dissection after a 12-year-interval: a case report]

Recurrence of spontaneous cervical internal carotid artery (ICA) dissection is not rare (1%/year) but bilateral recurrence affecting the same cervical ICA is rare, especially after a 12-year-interval. A 41-year-old man exhibited left hemiparesis and angiography revealed tapered stenosis of his right cervical ICA. Within 2 days, his hemiparesis improved. After 21 days, repeated angiography showed complete resolution of the once-stenosed right cervical ICA. He was discharged with slight left hemiparesis. The follow-up angiography performed after 18 months disclosed not only the recanalization of the right cervical ICA but also a new concentric stenosis of his left cervical ICA. Since he presented no new neurological deficit, he was treated with an antiplatelet agent. The angiography performed 14 months later revealed normalization of bilateral cervical ICA. After 12 years, at the age of 53, he presented with worsening of his left motor weakness. Also on this occasion, angiography revealed bilateral cervical ICA dissection and their spontaneous resolution. The anamnesis revealed that he had experienced the same ischemic symptoms, that is, hemiparesis, aphasia and their spontaneous resolution, when he was 24 and 37 years of age. These 4 episodes had some characteristics in common: occurrence in winter (from December to March), being preceded by moderate fever and upper respiratory tract infection. The pathogenesis of spontaneous cervical ICA dissection is unclear. From experience with this patient, we propose that the occurrence of spontaneous cervical ICA dissection might depend on a genetic predisposition and infection might play the role of a trigger.     

Bilateral medial medullary infarction

We present a case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging (MRI) and review 12 previously reported cases. We classify these 13 cases (including the present case) into two groups according to the extent of the ischemic region: type 1, the ischemic lesion developed from the medullary pyramid to the medial longitudinal fasciculus; type 2, the lesion was confined to the medullary pyramid.A 71 year old man presented with slight disturbance of consciousness, dysarthria, disturbance of leftward gaze, no gag reflex and tetraparesis. He developed nearly complete horizontal ophthalmoplegia. MRI revealed upper medial medullary infarction bilaterally that extended to the pontomedullary junction. We propose that the prognosis of type 2 bilateral medial medullary infarction is better than that of type 1. Furthermore, the prognosis of bilateral medial medullary infarction itself may be better than previously indicated.     

A case of juvenile cerebral infarction caused by bilateral anterior cerebral artery dissection]

A 38-year-old man was admitted to our hospital with headache, dysarthria and paraparesis. Brain CT and diffusion MRI disclosed cerebral infarction at bilateral anterior cerebral artery (ACA) territories. His symptoms and signs deteriorated in several days despite intensive antithrombotic therapy, resulting in right hemiparesis, akinetic mutism, memory disturbance, change of personality, urinary incontinence, forced grasping, and starting delay of speech and motion. Cerebral angiography demonstrated occlusion with contrast pooling at the right ACA A2 portion. Stenosis and dilatation were found at left ACA A2 portion. An intimal flap was also demonstrated on serial angiography. This case was diagnosed as cerebral infarction caused by dissection of bilateral ACA. Although no definite primary arteriopathy was demonstrated, bilateral dissection could be occurred simultaneously.     

Serial T2 short inversion time inversion recovery images in a patient with medullary hemorrhage]

A 52-year-old man was admitted to our hospital because of hypesthesia on the right side of his body. He had no medical history. On admission, he exhibited hypesthesia and disturbance of the touch and the vibratory sense on the right side of his body excluding the face. A brain T2* -weighted image revealed the a dot like lesion surrounded by an iso-signal lesion in the medial medulla oblongata. Therefore a diagnosis of medullary hemorrhage was made. Although a vascular malformation was considered as the cause of the hemorrhage, cerebral angiography did not reveal any vascular malformations. After admission, he developed left hypoglossal nerve palsy on day 6, and intractable hiccups on day 11. A T2* -weighted image and a FLAIR image disclosed edema surrounding the hematoma in the medial medullary lesion. T2* weighted images are useful for diagnosing and evaluating serial changes of medullary hemorrhage.     

A case of medial medullary syndrome detected by diffusion-weighted magnetic resonance imaging]

We report an 84-year-old woman with medial medullary syndrome diagnosed by diffusion-weighted magnetic resonance imaging (MRI). She was admitted because of left hemiparesis and hypesthesia. T2-weighted and diffusion-weighted MRI showed a high signal lesion at the right medial medulla oblongata 10 days after the onset. It is well known that diffusion-weighted MRI is useful for detecting supratentrial cerebral ischemic lesions in the extremely acute stage. However, to our knowledge, there have been only a few reports of diffusion-weighted MRI in patients with ischemic stroke of the medulla oblongata. Normal nerve fibers in the direction perpendicular to the motion-probing gradient (MPG) shows a high signal by diffusion-weighted MRI (anisotropy of apparent diffusion cofficient [ADC]). Normal nerve fibers in the pyramidal tract of medulla oblongata also shows a high signal when the MPG pulse is applied in the x and y directions. We solved this problem by using isotropic diffusion-weighted imaging and were able to detect ischemic lesion of medial medullary infarction in the acute phase.     

A rare case of subarachnoideal pneumocephalus after ear douche therapy

No detailed reports on pneumocephalus caused by any factors other than head trauma, and their courses accompanied with this disease have been so far available. We recently experienced a case of pneumocephalus complicated with severe clouding of consciousness, ocular deviation, and unilateral spatial neglect with the results being reported hereinafter. A 54-year-old man had often received ear douche therapy due to chronic sinusitis and tubal obstruction about 3 years before without any history of head trauma. On Jan. 6, 1984, sudden clouding of consciousness accompanying stiffness of the left arm occurred immediately after ear douche, and then he was transferred to our center. At admission, semicomatose, bilateral ocular deviation to the right, and left hemiparesis were observed. Plain skull X-ray films showed a retention of air in the frontal and temporal regions, while CT scan revealed air retention on the bilateral frontal region, bilateral temporal tip and suprasellar cistern. However, no abnormal findings were detected in the brain. Consciousness and hemiparesis recovered on the next day of hospitalization, however, the left hemispatial neglect still remained. This symptom was still observed on the 3rd day but disappeared by the 4th day of hospitalization. For clarifying its cause, cerebral angiography, CT scan and electroencephalography were then performed. CT scan revealed no anomalies in the brain, while cerebral angiography showed a cerebral circulation pattern in favor of the right internal carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Urinary retention associated with unilateral medullary infarction]

A 59-year-old man without any history of urinary disturbance, admitted to our hospital because of dysarthria and left hemiparesis. Diffusion weighted MR image of the brain of the 2nd hospital day showed left lateral medullary infarction. He also suffered from urinary disturbance which revealed to be the atonic bladder after the urodynamic study. Although the autonomic disturbance, such as Horner syndrome, is a well-known symptom in patients with lateral medullary infarction, few reports mentioned about the prevalence and the extent of urinary disturbance. The obstructive urinary disturbance observed in the present patient was thought to be caused by the unilateral lateral medullary infarction.