Restricted pain and thermal sensory loss in a patient with pontine lacunar infarction: a clinical MRI study

Pure sensory syndrome (PSS) is characterized by hemisensory symptoms without other major neurological signs. It was initially attributed to thalamic lacunar infarction, but several reports have shown the PSS can be due to small infarcts involving the posterior part of the internal capsula, the cerebral cortex and the brainstem. Paramedian and lateral pontine infarctions are associated respectively with lemniscal and spinothalmic (ST) sensory impairment. We describe a patient with an isolated impairment of the ST modalities caused by a segmental paramedian pontine infarction.     

Non-dominant hemisphere syndrome as a result of a right thalamic infarct: an anatomoclinical case

A 71 year old man had a massive left sensory deficit and hemiplegia, with left heminanopia, visual neglect and constructional apraxia. Moreover he experienced an extra-left arm and illusions of movements. 3 weeks later he suffered "thalamic" pain on left side; he died suddenly 6 weeks after the stroke. Post-mortem examination revealed: a) a right inner temporal and occipital infarction; b) a right thalamic infarction in the thalamogeniculate and paramedian territories; c) an infarction in the adjacent right internal capsule. Considering this case and pertinent literature on clinicopathological studies of right thalamic infarction, the authors suggest that a simultaneous ischaemia of thalamogeniculate and paramedian territories should be necessary to induce somatognosic and visuospatial disturbances.     

Aphonia as the only speech disturbance from bilateral paramedian thalamic infarction

We examined a 55-year-old right-handed woman showing transient coma, amnesia, mild right hemiparesis, vertical gaze impairment and aphonia without aphasia. CT-scanning revealed bilateral paramedian thalamic infarction in the territory of the thalamo-subthalamic paramedian arteries. Aphonia may occur as a consequence of thalamic lesions, but until now it has not been described as an isolated speech disturbance.     

Reduced sensorimotor inhibition in the ipsilesional motor cortex in a patient with chronic stroke of the paramedian thalamus.

OBJECTIVE: Unilateral or bilateral paramedian infarction in the region of the thalamus and upper midbrain may lead to hypersomnia. To determine whether unilateral infarction of the paramedian thalamus leads to changes in excitability of ipsilesional primary motor hand area (M1). METHODS: We describe a patient with chronic stroke of the right dorsomedian and intralaminar thalamic nuclei, who suffered from mild persistent hypersomnia. We studied the excitability of the right and left M1 with transcranial magnetic stimulation (TMS) in the patient, and in 10 healthy controls. RESULTS: In contrast to healthy controls, contralateral electrical stimulation of the median nerve failed to induce short-latency afferent inhibition (SAI) in the ipsilesional M1. Other measures of corticomotor excitability and somatosensory evoked potentials were normal. CONCLUSIONS: The selective loss of ipsilateral SAI in a patient with paramedian thalamic stroke suggests that during wakefulness, the intact paramedian thalamus facilitates the excitability of intracortical inhibitory circuits, which process thalamocortical sensory inputs in the ipsilateral M1. This preliminary finding suggests that measurements of SAI may provide a means of probing the integrity of some neural pathways, which are involved in the control of wakefulness and arousal. SIGNIFICANCE: In addition to the established role of the paramedian thalamus in arousal and memory, our observation suggests that thalamocortical projections from the paramedian thalamus contribute to the integration of sensory input at the cortical level during wakefulness.     

A case of postcentral infarction presenting discriminative sensory impairment limited to the distal leg on one side]

Presented is a case of postcentral infarction in a 70-year-old woman, which manifested as sensory disorders localized at the distal portion of the right lower extremity. Sensory disorders were characterized by the disturbances of discriminative sensation. Elemental senses were nearly normal. MRI revealed cerebral infarction localized at the superior portion of the postcentral gyrus and medial surface of the parietal lobe and the paracentral lobule of the left cerebral hemisphere. Carotid echography demonstrated stenotic lesions of the bilateral internal carotid arteries, suggesting that infarction of the cortical branch of the anterior cerebral artery due to artery-to-artery embolism was the cause of the condition. Cortical sensory disturbances due to lesions at the somatosensory area of the postcentral gyrus often appear on the upper extremities and face, and rarely occur as sensory disturbances that were localized in the distal portion of the lower extremities, as in this patient. The case suggests that it is important to keep in mind that sensory disorders that are localized in a single extremity with a distribution that suggests peripheral nerve lesions can be caused by cerebral cortical lesions.     

Monocular central dazzle after thalamic infarcts.

The authors observed a patient after he had ischemic strokes in both paramedian thalamic regions, which were more marked on the left side. Symptoms included dysphasia, vertical binocular diplopia, right-sided hemianopia, and a right-sided sensory and motor deficit, sparing the face. However, the most disturbing phenomenon was a painless, left monocular dazzle, which was the presenting symptom and also the only persisting symptom. This report shows that a thalamic lesion may be at the origin of central dazzle, and to the authors' knowledge, it is the first clinical observation of its monocular occurrence. It is conceivable that this dazzle was due to optic-trigeminal summation.     

Bilateral thalamic infarction. Clinical, etiological and MRI correlates

To determine clinical, behavioral, topographic and etiological patterns in patients with simultaneous bilateral thalamic infarction in varied thalamic artery territories, we studied 16 patients who were admitted to our stroke unit over a 7-year period. Patients with bithalamic infarction represented 0.6% of our registry which included 2,750 ischaemic stroke patients. On computed tomography and magnetic resonance imaging with gadolinium enhancement, there were 4 topographic patterns of infarction: 1) bilateral infarcts in the territory of paramedian artery (8 patients [50%]); 2) bilateral infarcts in the territory of thalamogeniculate arteries (3 patients [19%]); 3) bilateral infarcts involving territory of paramedian and thalamogeniculate arteries (3 patients [19%]); 4) bilateral infarcts involving territory of polar and thalamogeniculate arteries (2 patients [13%]). A specific clinical picture was found in up to 50% of the patients with bithalamic infarction. This included patients with bilateral paramedian infarction having disorder of consciousness, memory dysfunctions, various types of vertical gaze palsy and psychic changes. Bilateral sensory loss predicted accurately bilateral infarction in the territory of thalamogeniculate arteries. The main cause of bilateral thalamic infarction was small artery-disease, followed by cardioembolism. Cognitive functions in patients with bilateral paramedian infarction did not change significantly during the follow-up, in contrast to those with infarcts in varied arterial territories. Acute bilateral infarction involving both thalamus is uncommon, although they are often associated with specific neurologic-neuropsychological patterns, allowing diagnosis before radiological examination.     

Korsakoff's syndrome as a prominent feature of bilateral paramedian thalamic infarction--a case report

We reported the first Japanese case of bilateral paramedian thalamic infarction associated with prominent Korsakoff's syndrome. 53-year-old man suffered from semicoma on the morning of September 16th, 1988. After recovery of consciousness disturbance, neurological examination revealed vertical eye gaze palsy, areflexia of lower extremities, apathy with hypersomnia and amnesia. Amnesia was accompanied with prominent confabulation, disorientation and lack of insight into his own disability. While X ray-CT revealed only ambiguous low density area in the bilateral thalamus, MRI of horizontal section by short spin echo revealed symmetrical low signal area restricted in the paramedian area of bilateral thalamus, and that of coronal section revealed characteristic butterfly-shaped lesion. Left BAG revealed that both posterior thalamoperforating arteries showed type 3 variation of Percheron's classification which arisen from artery arcade bridging between both side of interpeduncular segment of posterior cerebral artery. He showed gradual improvement in apathy with hypersomnia and disorientation but not in Korsakoff's syndrome nor ophthalmoplegia.     

'Peduncular hallucinosis' following paramedian thalamic infarction

An 83-year-old man had the sudden onset of vivid formed hallucinations, agitation, and sleep disturbance suggesting "peduncular hallucinosis." A magnetic resonance scan revealed a right paramedian thalamic infarction with no abnormality of the cerebral peduncles or midbrain.     

Anatomy of sensory findings in patients with posterior cerebral artery territory infarction.

BACKGROUND: Posterior cerebral arteries (PCAs) supply the ventrolateral thalamic sensory nuclei and white matter sensory tracts to the somatosensory parietal cortex. Patients with PCA territory strokes often have visual, memory, cognitive, and sensory signs. Clinicoanatomic correlation of visual, cognitive, and memory functions are well defined but, to our knowledge, no systematic study has analyzed the anatomy of sensory abnormalities. OBJECTIVE: To assess the frequency and anatomic correlation of sensory symptoms and signs in patients with PCA territory infarction. PATIENTS AND METHODS: Sixty patients with hemispheral and hemispheral and deep PCA territory infarcts apparent on computed tomographic and magnetic resonance imaging scans were studied for the presence of sensory findings and location of infarcts. RESULTS: Sensory symptoms or signs were present in 15 (25%) of 60 patients. Among patients with sensory findings, 11 of 15 had infarcts in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries. The other 4 patients had no ventrolateral thalamic or white matter infarction but had severe proximal vascular occlusive lesions that could have caused temporary thalamic ischemia. One of these 4 patients had a medial thalamic infarct and transient hemisensory symptoms. Twelve patients had thalamic infarcts and no recorded sensory findings. Seven patients with thalamic infarcts (6 medial and 1 ventrolateral) had no sensory findings, and sensory findings could not be accurately assessed in 4 patients with ventrolateral and 1 patient with medial thalamic infarcts. CONCLUSIONS: All patients with PCA territory infarcts and sensory findings either had thalamic infarcts in thalamogeniculate or lateral posterior choroidal artery territory or had thalamic ischemia. Sensory findings in PCA territory infarction indicate ventrolateral thalamic ischemia.     

Cerebral infarction accompanied by dysgeusia--a clinical study on the gustatory pathway in the CNS]

Dysgeusia was investigated in 11 patients with thalamic infarction and 13 patients with corona radiata infarction to locate the gustatory pathways based on the sites of the lesions. Dysgeusia was present in 4 out of 11 patients with thalamic infarction and 3 out of 13 patients with corona radiata infarction. The dysgeusia was contralateral to the lesion in all these patients. Cheiro-oral syndrome was observed as a complication in 2 patients each from both groups. The responsible lesion was located on the medial side of the ventral posterolateral (VPL) nucleus and the ventral posteromedial (VPM) nucleus in the patients with thalamic infarction who developed dysgeusia, and was located posteriorly to the corona radiata in the other group. In the patients without gustatory disturbance, on the other hand, the lesions showed no such spread. These findings suggest that the gustatory pathway ascends contralaterally in the cerebral hemisphere and that the pathway from the thalamus projects to the cerebral cortex via the posterior part of the corona radiata. It is also suggested that the pathways in the thalamus and corona radiata are very close to the sensory fibers from the mouth and hands projecting to the sensory area.     

Pure thalamic infarctions: Clinical findings

Our purpose in this study was to evaluate and review the risk factors, clinical profiles, and neuropsychologic abnormalities in patients with pure thalamic infarctions and to describe the clinical syndromes according to the thalamic arterial territory involved. We studied all patients with acute thalamic stroke admitted to our stroke unit over a 5-year period. We performed magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) on all patients. We classified patients into 4 thalamic artery territory subgroups based on MRI findings: thalamogeniculate, paramedian, polar, and posterior choroidal. Patients with pure thalamic infarction represented 2.4% of patients with ischemic stroke in our registry. There were 59 patients (39 men and 20 women; mean age, 62 ± 13 years) with thalamic infarctions that were confirmed by MRI. The main cause of thalamic infarction was small artery disease (75%). Hypertension (68%), hypercholesterolemia (29%), and diabetes mellitus (27%) were the most frequent risk factors. Hemisensory loss with or without motor and neuropsychologic deficit is highly associated with thalamogeniculate infarction, the most frequent type of thalamic stroke (51%). Paramedian infarction was the second most common type of thalamic infarction (34%) and is characterized by several neuropsychologic, oculomotor, and consciousness disturbances. Frontal-like syndrome with sensory motor findings is common in polar artery territory infarction (10%). Visual field defect is associated mainly with infarctions in the territory of the posterior choroidal artery (5%), probably caused by involvement of the lateral geniculate body. Approximately two thirds of the patients returned to their previous normal life. Cognitive deficits in patients with bilateral paramedian infarction persisted during the follow-up period, contrary to the other thalamic stroke subtypes. No patient died during follow-up. Acute thalamic stroke is a specific clinical picture that accurately predicts a small artery disease in the posterior circulation. The 4 arterial thalamic territories correspond well clinically to 4 different syndromes. Acute thalamic infarction appears to predict an overall good clinical recovery.     

A case of Werdnig-Hoffmann disease showing extensive sensory involvement after prolonged mechanical ventilation

A 5-year-old boy with Werdnig-Hoffmann disease (WHD), who had been mechanically ventilated for the majority of his life, was examined pathologically. In addition to the classic features of WHD, extensive sensory involvement, including pronounced glial bundle formation in the posterior nerve root, severe demyelination of the posterior column in the whole spinal cord and thalamic neuronal loss were observed. Mechanical ventilation for 5 years prolonged the patient's survival beyond its natural course and produced the unusual pathological findings such as the phrenic motoneuronal loss and severe diaphragmatic and intercostal muscle atrophy. This also appeared to be responsible for the extensive sensory involvement. Data from this case and from previous reports show that WHD is a potential multisystem disorder affecting primarily, but not exclusively, the motor system. We observed marked neuronal accumulation of eosinophilic intracytoplasmic granules in the oculomotor nucleus, substantia nigra, locus ceruleus and nucleus raphe pontis, which appeared as intramitochondrial electron-dense granules on electron-microscopy and myoglobin-positive granules by immunostaining.     

Intermediate medullary infarction: a case report]

A 68-year-old man presented with right eye pain and vertigo. Thereafter, he gradually leaned rightward, then laid down. He felt nausea and vomited. His right upper eyelid drooped and he felt dysethesia of the right hand. On neurological examination, ptosis of his right eye with slightly miotic right pupil, paresis of the right soft palate and hoarseness were noted. Arm deviation test demonstrated rightward deviation. He presented sensory ataxia of the right upper and lower extremities: finger nose test showed mild dysmetria of the right upper extremity, heel knee test demonstrated dysmetria of right lower extremity and these findings worsened when he closed his eyes. He showed mild bending of his bilateral ring and little fingers when he did rapid alternative movement. He leaned rightward when he sat and closed his eyes. Position sense of his right upper and lower extremities was decreased and sometimes he could not answer correctly when asked on which direction his finger pointed. Pinprick sensation was mildly decreased on the left side not including the face. Touch and vibration sense were normal. SEP findings on upper and lower extremity stimulation were normal. MRI of the brain showed T2 high intensity and partially T1 low intensity lesion at the right medulla (Figure). MR angiography showed no apparent lesion of major arteries such as dissection of the vertebral arteries. He complained and presented with hiccup initially. On MRI, the lesion was thought to involve the spinothalamic tract, medial lemniscus and inferior olivary nucleus. Ambiguus nucleus was in the lesion and solitary nucleus near the lesion. There is no report that seems to describe clinical features of a lesion like that in this case. Intermediate medullary infarction may present dissociated sensory disturbance like Brown-Sequard syndrome and position sensory disturbance without disturbance of vibration sense.     

Paramedian thalamic and midbrain infarcts associated with palilalia

We report a case with paramedian thalamic and midbrain infarcts associated with palilalia. A 62-year-old man fell into a comatose state, and was admitted to an emergency hospital. Two days later, his consciousness level began to improve. Neurological examination revealed bilateral cerebellar ataxia, oculomotor nerve palsy, lack of spontaneity, and amnesia. Deep tendon reflexes were normal on all extremities, and no muscular weakness was observed. Babinski sign was noted on the right side. Muscle tone was decreased. No sensory disturbance was found. Two months later, he began to show compulsive repetition of syllables, words, or phrases, and was transferred to our hospital. He involuntarily repeated one syllable or a word five to ten times in spontaneous speech, repetition of phrases being not so frequent as that of syllables or words. This speech abnormality was considered as palilalia, which Souques first reported in 1908. The palilalia of this patient was rarely noted when he repeated words spoken to him by the examiner. As he spoke, the rate of speech gradually increased, the loudness reduced, and finally he began to whisper (palilalie aphone). The palilalia continued for four months. MRI showed infarcts in the medial thalami, subthalamic and midbrain on both sides. Auditory brainstem response showed delayed latency of bilateral V waves, and EEG revealed bilateral theta waves. In this patient no lesion other than thalamus, subthalamus and midbrain was detected by MRI. It is suggested that bilateral lesion of the thalami and their projection areas caused palilalia in this patient.     

Clinical manifestation of small thalamic hemorrhage

CT scan is useful for the simultaneous evaluation of the relation between the thalamic lesions and the clinical manifestations. According to CT findings, twenty-three patients with thalamic hemorrhage measuring less than 2 cm in size could be classified into 4 groups: 1) anterior group--hematoma located in the anterior nuclear group, 2) medial group--hematoma located in the medial nuclear group, 3) lateral group--hematoma located in the lateral nuclear group close to the internal capsule, 4) posterior group--hematoma located in the pulvinar. The clinical manifestations of both the anterior and medial groups were characterized by the disturbance of consciousness followed by the mental impairment; the lateral group, by the hemiparesis or hemiplegia with the sensory disturbance, and the posterior group, especially with left thalamic lesions, by the speech disturbance. The motor palsy in cases of thalamic hemorrhage differed from that of putaminal hemorrhage: the patients with thalamic hemorrhage could move their fingers despite being unable to move their shoulders and elbows, or the motor weakness was more severe in their lower extremities than in their upper ones. As the sensory disturbance, the sensory impairment (hypesthesia) was frequently associated with the numbness (dysesthesia). The prognosis of motor palsy, ocular manifestations, and speech disturbance was good, whereas that of sensory and mental disturbance was not always good.     

A case of motor and sensory polyneuropathy with retinitis pigmentosa and diffuse idiopathic skeletal hyperostosis]

We here report a 53-year-old man who presented with motor and sensory polyneuropathy, retinitis pigmentosa and diffuse idiopathic skeletal hyperostosis (DISH). He had a 15-year history of diabetes mellitus (DM). Visual impairment appeared at 17 years of age. Since age 47, he showed a slowly progressive sensory impairment and muscle weakness of the extremities. On neurological examination, retinitis pigmentosa and severe muscle atrophy, muscle weakness and sensory disturbance of all modalities in the distal portions of all four extremities were observed. Deep tendon reflexes were absent. A plain X-P showed diffuse ossification of the spinal and extraspinal ligaments. The motor nerve conduction velocities were severely reduced and no sensory nerve action potentials were evoked. The CSF examination revealed an increased protein level without pleocytosis. The sural nerve biopsy showed a marked onion bulb formation and a loss of the myelinated nerve fibers, which could not be solely explained by DM. As the phytanic acids levels, beta-lipoprotein, lactate and pyruvate in the sera were within the normal ranges, Refsum disease, Bassen-Kornzweig syndrome and mitochondrial diseases were unlikely in this patient. The presence of demyelinating and axonal polyneuropathy in this patient may have been caused by a common metabolic disturbance which produced both retinitis pigmentosa and DISH.     

Hemiparesthesias in lacunar pontine ischemic stroke

Isolated paresthesia, or paresthesia not accompanied by sensory and/or motor deficits, is an extremely rare manifestation of a cerebrovascular accident. Lacunar pure sensory stroke (PSS) confined to thalamus is characterized by persistent or transient numbness, tingling, pain, burning, or another unpleasant sensation on one side of the body. However, in this condition a sensory loss to all primary modalities in the contralateral face and body is very often encountered. Also previous reported cases of PSS due to lacunar stroke in regions other than thalamus are characterized by the presence of sensory loss together with positive sensory symptoms, none of them reporting isolated paresthesia as the only clinical feature of PSS. We present a case of isolated paresthesia as only clinical manifestation of a lacunar PSS involving both trigeminal and medial lemniscus in dorsal paramedian pontine region. A PSS manifesting with isolated paresthesias may be secondary not only to a thalamic lacunar stroke, but also to a small ischemic lesion confined to both trigeminal and medial lemniscus in dorsal paramedian pontine region.     

Neuropsychological profile of bilateral paramedian infarctions: Three cases

Introduction: The thalamus is one of the strategic diencephalic structures of the human brain. The artery of Percheron, an asymmetrical common trunk arising from a P1 segment of the posterior cerebral artery, is a peculiar presentation of the three variants involved in the irrigation of the paramedian thalamic territory. Occlusion of this artery results in bilateral median thalamic infarction. The paramedian syndrome includes an acute loss or reduction of consciousness, often associated with oculomotor and neuropsychological disturbances. Patients and methods: We present three cases of bilateral paramedian thalamic infarction with onset of acute coma, followed by fluctuations in the level of consciousness, memory, and behavioural alterations. A neuroradiological study with MRI identified individual thalamic nuclei, and a complete neuropsychological study was performed one month after onset of ictus. Results: One of the patients showed severe memory and executive function impairments without improvement of vertical gaze palsy. The other two patients presented with mild executive dysfunction with complete resolution of neurological symptoms. Neuroimaging results showed a bilateral lesion of the dorsomedial nuclei in the three patients. Conclusions: Severe amnesia has been associated with an affection of the structures of the paramedian thalamic territory. Presently, the role of the dorsomedial nucleus remains controversial, with the suggestion that memory deficits observed in this type of lesion could be secondary to executive function deficits. In our case, the patient with the most severe dysexecutive deficit presented the most severe memory impairments.     

Thalamic transitory ischemic attacks presenting as Jacksonian sensory march

Spreading somatosensory symptoms appearing as Jacksonian sensory march are usually considered to be due to an epileptic seizure. We report on three cases in which these symptoms were caused by thalamic ischemia. Two patients presented with stereotypically recurring hemiparesthesias lasting 2–5 min that gradually spread from the face to the arm and leg on one side. A first cerebral magnetic resonance imaging including DWI was negative in both cases, whereas new thalamic infarctions appeared on repeated imaging when clinical symptoms remained. A third case with a thalamic ischemia did not show recurring events, but also presented with purely sensory spreading symptoms. In all three cases EEG and cardiovascular diagnostics revealed normal results. Pure sensory stroke has previously been described as a result of ischemia of the thalamus or the internal capsule presenting as a sudden onset hemisensory deficit, but spreading symptoms have rarely been reported. According to our observations, thalamic TIAs are an important differential diagnosis of somatosensory epileptic auras presenting with Jacksonian sensory march which require a different clinical management.