Pure motor hemiparesis due to non-hypertensive putaminal haemorrhage

Summary The syndrome of pure motor hemiplegia (PMH) has been traditionally regarded to be due to lacunar infarcts at various places in the brain. Recently, attention has been drawn towards various other aetiological factors which have been responsible for this clinical presentation. PMH as a result of hypertensive putaminal haemorrhage is extremely uncommon. A case of PMH as a result of non-hypertensive putaminal haemorrhage is described.     

Serial changes in motor and somatosensory evoked potentials in putaminal haemorrhage

Little is known about evoked potential changes in putaminal haemorrhage. In this study, somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) have been serially evaluated and their role in the prognosis of putaminal haemorrhage is now reported. Nineteen patients with CT- or MRI-proven putaminal haemorrhage were examined after a mean duration of 13 days (range 2–30); there were 4 females and 9 males, ranging in age between 25 and 70 years. The haematomas were of medium size in 13 and large or small in 3 patients each. The changes in the clinical picture and the SEPs and MEPs were evaluated on admission, and after 30 and 90 days. Central motor conduction time (CMCT) could not be recorded in 13, but was prolonged in 2 and normal in 4 patients. Median SEPs revealed the absence of near field potentials in 11 and prolongation of N9–N20 conduction time in 1 patient. In the follow-up period MEP and SEP abnormalities only changed in 5 patients; MEPs changed in 4 and SEPs in 2. The period of normalisation of MEPs ranged between 1 and 6 months. CMCT correlated with motor and N9–N20 conduction time with sensory impairment. Eight patients had poor, 6 partial and 5 complete recovery. Power, sensation, CMCT, and size and location of haematoma made positive contributions to recovery.     

Pure motor hemiplegia secondary to a saccular basilar artery aneurysm

Pure motor hemiplegia is the most commonly encountered lacunar syndrome and is classically associated with small infarctions in the contralateral internal capsule or basis pontis. Pure motor hemiplegia has also been observed secondary to a wide variety of other vascular and nonvascular focal central nervous system processes. We describe a patient with pure motor hemiplegia associated with a saccular basilar artery aneurysm causing a lacunar infarction of the cerebral peduncle.     

Lacunar infarction as an embolic complication of cardiac and arch angiography

BACKGROUND: Lacunar infarcts are small, deep cerebral infarcts resulting from occlusion of small, penetrating cerebral arteries. They are most commonly associated with hypertension. Cardiac sources of embolization are sometimes present in patients with lacunes, but direct proof of a causal relationship is lacking. This report attempts to support the contention that emboli can cause lacunar syndromes and lacunar infarction. CASE DESCRIPTIONS: We report two cases of pure motor hemiplegia, each of which developed while the patient was undergoing cardiac or aortic arch angiography. Neither patient had a history of previous transient ischemic attack or stroke. Initial computed tomography of the brain was normal in each. Repeat computed tomography in one confirmed a small, low-density lesion in the posterior limb of the internal capsule on the side appropriate to the patient's symptoms and remained normal in the second patient. CONCLUSIONS: These two cases offer evidence that the classic lacunar stroke syndrome of pure motor hemiplegia can occur on an embolic basis.     

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.     

Type I familial amyloid polyneuropathy and pontine haemorrhage

A Portuguese female, aged 47 years, who had emigrated to Spain, was admitted to the hospital in 1991 for pontine haematoma. The patient, four siblings and her father were affected by a peripheral neuropathy, indicating autosomal dominant inheritance. The patient presented in the 2nd decade with sensory and motor neuropathy beginning in the lower extremities. Alternating constipation and diarrhoea, and urinary incontinence became uncontrollable. She had to be colostomised, and, eventually, confined to a wheelchair from the age of 43. Neurological examination showed bilateral facial involvement, and severe signs of sensory and motor peripheral neuropathy, and later right hemiplegia. There were abnormalities of atrial rhythm and left bundle branch block. Computerised axial tomography and magnetic resonance images demonstrated left-sided pontine haemorrhage. Nerve conduction studies revealed severe diminution of motor conduction velocity and absence or reduction of amplitude of sensory and motor action potentials. Inanition and a respiratory infection led to her death. Clinical diagnosis was type I familial amyloid polyneuropathy (FAP). Postmortem examination demonstrated amyloid deposits in peripheral nerves, including spinal roots and cranial nerves, leptomeninges, thyroid, breasts, heart, adrenal glands, kidneys, intestines, pancreas, and meningeal and some pontine vascular structures. Advanced pontine haematoma was verified. Cerebral haemorrhage usually occurs with cerebrovascular amyloidosis, but exceptionally with FAP. A minority of patients presenting with CNS haemorrhage showed arteriovenous malformation or embolism [Da Silva Horta and Dias Coelho (1960) Arch de Vecchi Anal Patol Med Clin 31=163–172]. However, amyloid deposition in some small pontine vessels could have played a role in the pathogenesis of haemorrhage in the present case.     

Computed tomography and pure motor hemiparesis

Computed tomography (CT) was abnormal in 75% of 33 patients with pure motor hemiparesis (PMH). In 13 cases, lesions were detected in the capsular region; 10 were consistent with infarction, and 3 were of increased density consistent with hemorrhage. Seven had other vascular disorders, and four had nonvascular conditions. Of 20 patients with PMH with normal electroencephalogram (EEG), isotope scan, and cerebrospinal fluid, 11 had CT evidence of a lesion in the internal capsule-corona radiata region. In patients with PMH with normal CT, recovery was more complete and rapid than in those with CT evidence of a vascular lesion. In 5 cases, CT showed a capsular lesion, although the patients had never had any neurologic deficit.     

Motor dysfunction on the nonhemiplegic side in patients with intracerebral haemorrhage

This study was undertaken to evaluate the motor dysfunction on the nonhemiplegic side in patients with acute intracerebral haemorrhage (ICH) and correlate these with radiological and motor evoked potentials findings. 28 patients (23 males, 5 females), with CT proven ICH within 10 days of ictus were subjected to clinical evaluation and central motor conduction studies (CMCT) of upper limbs. The patient's age ranged between 28 and 84 years. Motor signs on the nonhemiplegic side were present in 17 patients in the form of increased tone (10), hyperreflexia (13) and extensor plantar response (10). Sixteen of these patients had severe weakness on the hemiplegic side. Most of the patients had putaminal haemorrhage (13) and thalamic and lobar haemorrhage was seen in 2 patients each. The motor dysfunction on the nonhemiplegic side correlated with midline shift but not with the size of haematoma. CMCT findings correlated with motor signs on the nonhemiplegic side in 6 patients. In the patients without any signs on the nonhemiplegic side, CMCT was normal. Out of 17 patients with motor dysfunction on the nonhemiplegic side 9 revealed improvement in CMCT at 1 month followup. The patients with CMCT abnormalities on the nonhemiplegic side either died (2) or had poor outcome (9). Motor dysfunction on the nonhemiplegic side may be due to tentorial herniation and suggests a poor outcome.     

白质纤维束示踪成像技术在高血压脑出血中的初步应用

目的探讨白质纤维束示踪成像技术在高血压脑出血中的临床应用价值。方法对我院8例急性期情况稳定的高血压脑出血患者进行磁共振弥散张量成像,应用日本东京大学的Volume-one1.72和Diffusion Ten-sor Visualizer(dTV)软件进行三维白质纤维束示踪成像,观察以内囊为主的白质纤维束的压迫、推移、破坏情况。结果8例患者均行磁共振弥散张量成像并行内囊白质纤维束示踪成像,可清楚看到内囊白质纤维束受血肿压迫、推移、破坏情况,由患侧内囊追踪到的相对纤维束条目数少于健侧内囊(P<0.005)。结论白质纤维束示踪成像技术可以清楚显示高血压脑出血后内囊白质纤维束的受累情况。     

Spastic pure motor monoparesis

Pure motor hemiplegia (PMH) is, in most cases, caused by a lacunar infarction. However, pure motor monoparesis (PMM), i.e., isolated motor involvement with spasticity in one limb, has drawn little attention. We studied prospectively 5 patients with PMM and found that it was always due to a mass lesion in the contralateral superficial cerebral hemisphere. Our observation suggests that PMM should not be regarded as simply a variant of PMH.     

Asymmetrical myelination of the posterior limb of the internal capsule in infants with periventricular haemorrhagic infarction: an early predictor of hemiplegia

AIM: To prospectively assess the predictive value of asymmetrical myelination on MRI of the posterior limb of the internal capsule (PLIC) in newborn infants with an intraventricular haemorrhage (IVH) associated with unilateral haemorrhagic parenchymal involvement (PI), for subsequent development of a hemiplegia. METHODS: 12 preterm infants (GA 25-36 wks) and 4 full-term infants were studied. Using cranial ultrasound (US), the pre-term infants were diagnosed to have an IVH with unilateral PI. The term infants presented with a porencephalic cyst (PC) on the first postnatal US, following an antenatal IVH with PI. MRI was performed at 40 wks postmenstrual age in the pre-term infants and during the first 2 weeks of life in the full-term infants, using a 1.5T magnet. Using an inversion recovery sequence, the myelination of the internal capsule was recorded as normal, abnormal or equivocal. Neurological assessment > or = 12 months disclosed the presence of a hemiplegia or asymmetry in tone pattern. RESULTS: All 4 cases with a normal internal capsule had a normal outcome in spite of the development of a PC. All 9 cases with an abnormal PLIC developed a hemiplegia, while 1 of the 3 cases with an equivocal PLIC is normal on neurological assessment, one developed a mild asymmetry in tone and 1 a mild hemiplegia. CONCLUSION: While a symmetrical signal intensity within the internal capsule on MRI, performed at 40 weeks PMA, in infants with an IVH and unilateral PI appears to be strongly related to a normal outcome, an asymmetrical PLIC is an early predictor of future hemiplegia.     

A case of pure motor monoparesis due to pontine infarction

Pure motor hemiplegia (PMH) is a common manifestation of lacunar infarction. However, pure motor monoparesis (PMM), isolated corticospinal tract deficits confined to one limb, have received little attention. We observed a patients in whom the clinical feature was compatible with PMM and discussed the possible pathomechanism of PMM.     

Evaluation of brain dysfunction in hypertensive putaminal hemorrhage with multimodality evoked potentials

Changes in multimodality evoked potentials (MEP's), consisting of somatosensory evoked potentials (SEP's), visual evoked potentials (VEP's), and auditory evoked brainstem responses (AEBR's), were studied in 36 patients with hypertensive putaminal hemorrhage to ascertain the relation among areas and distribution of brain dysfunction, the size of hemorrhage on computerized tomographic scan, and the clinical outcome. Among MEP's, SEP's were most significantly involved in all patients. Abnormalities in VEP's and AEBR's remained mild or moderate when the hemorrhage did not extend to the diencephalon. If SEP's were normal or mildly abnormal, they improved early the ictus. These patients did well clinically. If SEP's were absent, the patients had poor outcome even when the hemorrhage was small and located outside the internal capsule. In contrast, deterioration or persistence of MEP's indicated secondary insult to the brain and poor patient outcome. Early and serial MEP studies are useful in evaluating primary and secondary brain dysfunction and in predicting patient outcome in hypertensive putaminal hemorrhage.     

Isolated hemiataxia after supratentorial brain infarction.

Acute isolated hemiataxia is in most cases due to infratentorial (cerebellar) stroke. It has only twice been described in supratentorial stroke--namely, after thalamic infarction and a capsular haemorrhage. Three patients with isolated hemiataxia after a supratentorial brain infarct are described. These patients were seen in a period of five years during which 899 patients with a first supratentorial brain infarct were registered. Clinically the hemiataxia was of the cerebellar type. In two patients, CT and MRI showed a small, deep (lacunar) infarct restricted to the posterior limb of the internal capsule, a site not previously reported in isolated hemiataxia. The third patient had a small, deep (lacunar) infarct in the thalamus extending into the adjacent posterior limb of the internal capsule. Isolated hemiataxia after a supratentorial brain infarct is a very rare clinical stroke syndrome. The cerebellar type hemiataxia was most likely caused by interruption of the cerebellar pathways at the level of the internal capsule. Our cases confirm prior observations that the cerebellar pathways run through the posterior part of the posterior limb of the internal capsule separately from the motor and sensory pathways.     

Central motor conduction studies in internal capsule and corona radiata infarction

Clinical and evoked-potential studies in internal capsule and corona radiata infarction are lacking. We report the results of a clinical and central motor conduction time (CMCT) study in 16 patients with internal capsule and 17 with computed tomography (CT)-proven corona radiata infarction. Patient’s outcome was defined at the end of 3 months on the basis of the Barthel Index score. Four patients with type A capsular infarction (middle third of posterior limb of internal capsule) all had severe weakness, while 2 also had persistently unrecordable CMCT and poor outcome. Twelve patients with type B internal capsular infarction (genu, anterior limb, anterior or posterior third of posterior limb) had a milder degree of weakness, and CMCT was recordable in 9. At 3 months’ follow-up, however, CMCT was recordable in all 12 patients. All of these patients had a partial (n = 4) or complete (n = 5) recovery. Thirteen patients with type A corona radiata infarction (middle third of corona radiata) had more pronounced weakness, and CMCT was unrecordable in all of these patients except 1 on initial examination. Follow-up after 3 months was possible in 8 patients, and CMCT became recordable in 3. One of these patients had complete, 3 partial, and 4 poor recovery. In type B corona radiata infarction (anterior or posterior third of corona radiata), the clinical signs and CMCT did not follow a regular pattern. Clinical and CMCT abnormalities in internal capsular infarction followed a more predictable pattern compared with those in corona radiata infarction. A less predictable pattern of weakness and CMCT change in corona radiata infarction may be attributed to a less definite organisation of motor pathways compared with the internal capsule. Received: 13 January 1997 Received in revised form: 5 June 1997 Accepted: 27 June 1997     

Characteristics of intracranial aneurysms and subarachnoid haemorrhage in patients with polycystic kidney disease

Background and Purpose: Subarachnoid haemorrhage is a common cause of death in patients with autosomal dominant polycystic kidney disease (ADPKD), but little is known about specific characteristics of subarachnoid haemorrhage and intracranial aneurysms in this group of patients. We performed a systematic review on site, size and number of aneurysms, age at time of rupture, gender, and family history in patients with ADPKD and intracranial aneurysms. We also studied the frequency of ADPKD in patients with subarachnoid haemorrhage treated in our hospital. Methods: We performed a MEDLINE search and checked the reference lists of all relevant publications to identify all articles published from 1980 to 2000 on intracranial aneurysms or subarachnoid haemorrhage in ADPKD. We studied our database of patients with subarachnoid haemorrhage treated between 1978 and 1999 for the presence of ADPKD. Results: We included 53 articles on 369 ADPKD patients (139 [54 %] women) with 462 intracranial aneurysms. Of the 273 aneurysms with specified locations 105 (38 %) were located on the middle cerebral artery in and on the anterior communicating artery in 83 patients (30 %). In 253 patients with data about relatives, the family history was positive for intracranial aneurysms or subarachnoid haemorrhage in 102 (40 %). The average age at which subarachnoid haemorrhage had occurred in 258 was 41 years; of 158 in whom the gender was given; 96 (52 %) were women. Of the 160 patients with data on outcome, 69 (43 %) had died as the result of the subarachnoid haemorrhage. Of the 1147 patients treated for aneurysmal subarachnoid haemorrhage in our institution (mean age 53 years; 65.5 % women), 5 (0.44 %) had ADPKD. Conclusions: Compared with data on patients without ADPKD, subarachnoid haemorrhage in patients with ADPKD occurs not only often in a familial setting of subarachnoid haemorrhage, but also at an earlier age and more often in men. In patients with ADPKD, the most frequent site of aneurysms is the middle cerebral artery. The proportion of patients with ADPKD among all patients with subarachnoid haemorrhage is very small. Received: 17 April 2002, Received in revised form: 11 October 2002, Accepted: 16 October 2002 Correspondence to Professor Gabriel J. E. Rinkel     

Lower limb SSEP changes in stroke-predictive values regarding functional recovery

OBJECTIVE: To assess the predictive value of lower limbs somatosensory evoked potentials (SSEPs) in the acute phase of stroke. MATERIALS AND METHODS: 94 stroke patients (mean age: 61.2; S.D.: 11.8; 43 women) were included. Computed tomography confirmed diagnosis was cortical middle cerebral artery (MCA) infarction in 35, subcortical MCA in 11, and mixed in 25. By size, infarctions were large (29), limited (33), and lacunar (9). Thalamic haemorrhage was found in eight patients, putaminal in seven, small capsular in two, massive in two and lobar in four patients. All patients presented with hemiparesis (54) or hemiplegia (40), pure in five and combined with hemihypesthesia in 89. Tibial nerve SSEPs were recorded early in the course of the disease (up to third day). SSEP parameters (presence/absence of SSEP, absolute P40 latency, amplitude and amplitude ratio-affected/healthy side of P40-N50) were evaluated and compared with motor ability using the Medical Research Council (MRC) scale, and daily living activities using Barthel index (ADLB) followed for 3 months after stroke. Disability was assessed after the Rankin scale. RESULTS: The absolute amplitude of P40 has moderately strong correlation with Barthel index (r=0.63) and nearly moderate (r=-0.46) with Rankin scale at 3 months. P40 ratio exhibits weaker correlations with clinical outcome parameters. The combination of SSEP abnormalities and MRC has stronger predictive value than MRC alone (P<0.0001 vs P<0.03). CONCLUSIONS: Tibial SSEP investigation early in stroke, independently or combined with muscle power assessment, significantly increases prognostic capability.     

Haemorrhagic pure motor stroke

To describe the clinical characteristics of haemorrhagic pure motor stroke (PMS). Twelve patients with haemorrhagic PMS were identified. Haemorrhagic PMS accounted for 3.2% of all cases of pure motor hemiparesis ( n  = 380) and 3.3% of intracerebral haemorrhage ( n  = 364) entered in the database. When compared with PMS of ischaemic origin, patients with haemorrhagic PMS were more likely to be younger (62.2 vs. 75.2 years, P  = 0.003) and to have headache (33% vs. 6.3%, P  =0.007) and thalamus involvement (25% vs. 2.4%, P  = 0.005). Limb weakness (100% vs. 74.1%; P  = 0.03), involvement of the internal capsule (50% vs. 17.3%, P  = 0.012) and symptom free at discharge (25% vs. 3.7%, P  = 0.012) were significantly more frequent in patients with haemorrhagic PMS than in the remaining cases of haemorrhagic stroke, whereas nausea and vomiting (0% vs. 25.9%, P  = 0.03), altered consciousness (0% vs. 42.9%, P  = 0.001), sensory symptoms (8.3% vs. 46.9%, P  =0.007) and ventricular haemorrhage (0% vs. 26.1%, P  = 0.028) were significantly less frequent. Haemorrhagic PMS is a very infrequent stroke subtype. Headache at stroke onset may be useful sign for distinguishing haemorrhagic PMS from other causes of lacunar stroke. There are important differences between haemorrhagic PMS and the remaining intracerebral haemorrhages.     

A stainless steel sheath for endoscopic surgery and its application in surgical evacuation of putaminal haemorrhage

A stainless steel tube was used as an endoscope sheath in combination with a working channel endoscope to evacuate hypertensive putaminal intracerebral haematoma (ICH). A frontal entry point ipsilateral to the haematoma was selected for insertion of the sheath. From January to June 2004, seven patients with putaminal ICH underwent endoscopic surgery in our hospital. There were no surgical complications. Haematoma evacuation rates were greater than 90% (median of 93%). Six patients (87%) regained consciousness within one week. Six patients, including four who had no residual disability and two who had moderate disability, were able to function independently. One patient remained in a persistent vegetative state at clinical follow-up after 6 months. Use of a stainless steel endoscopic sheath combined with working channel endoscopy via a frontal approach facilitates evacuation of putaminal ICH.     

Pure motor hemiparesis due to hypertensive putaminal haemorrhage

A hypertensive woman presenting as pure motor hemiparesis with rapid and complete recovery from the neurological deficit is described. The probable aetiology was primary hypertensive putaminal haemorrhage, as revealed by CT scan. This rare presentation has been described only once earlier and emphasizes the value of CT scanning as a tool for diagnosis of such cases.