Persistent recurrence of hypomania and prosopoaffective agnosia in a patient with right thalamic infarct.

The authors report a 63-year-old man with a history of brief isolated manic episodes who became persistently hypomanic after a small right thalamic infarct. Detailed behavioral and neuropsychologic assessment were performed 18 months after the stroke and revealed a prosopoaffective agnosia as the foremost cognitive disorder, i.e., an impairment in the identification of emotional facial expressions with preserved discrimination of facial identity. Difficulties in reasoning on humorous material and other signs of mild right hemisphere dysfunction were present, but other perceptual, frontal and abstract-reasoning cognitive functions were unimpaired. Prosopoaffective agnosia has not been reported previously in thalamic lesions or in primary or secondary mania. The authors discuss the hypothetical relationships between a right hemisphere deficit in processing emotions and relapsing of the patient's hypomanic behavior.

Pure amnesia after unilateral left polar thalamic infarct: topographic and sequential neuropsychological and metabolic (PET) correlations.

A 54-year-old patient who had an isolated small polar thalamic infarct and acute global amnesia with slight frontal type dysfunction but without other neurological dysfunction was studied. Memory improved partially within 8 months. At all stages the impairment was more severe for verbal than non-verbal memory. Autobiographic recollections and newly acquired information tended to be disorganised with respect to temporal order. Procedural memory was unaffected. Both emotional involvement and pleasure in reading were lost. On MRI, the infarct was limited to the left anterior thalamic nuclei and the adjacent mamillothalamic tract. The regional cerebral metabolic rate of glucose (measured with PET) was decreased on the left in the thalamus, amygdala, and posterior cingulate cortex 2 weeks after the infarct, and in the thalamus and posterior cingulate cortex 9 months later. These findings stress the specific role of the left anterior thalamic region in memory and confirm that longlasting amnesia from a thalamic lesion can occur without significant structural damage to the dorsomedial nucleus. Furthermore, they suggest that the anterior thalamic nuclei and possibly their connections with the posterior cingulate cortex play a role in emotional involvement linked to ipsilateral hemispheric functions.

Sensory syndromes in parietal stroke.

We studied 20 patients with an acute parietal stroke with hemisensory disturbances but no visual field deficit and no or only slight motor weakness, without thalamic involvement on CT or MRI and found three main sensory syndromes. (1) The pseudothalamic sensory syndrome consists of a faciobrachiocrural impairment of elementary sensation (touch, pain, temperature, vibration). All patients have an inferior-anterior parietal stroke involving the parietal operculum, posterior insula, and, in all but one patient, underlying white matter. (2) The cortical sensory syndrome consists of an isolated loss of discriminative sensation (stereognosis, graphesthesia, position sense) involving one or two parts of the body. These patients show a superior-posterior parietal stroke. (3) The atypical sensory syndrome consists of a sensory loss involving all modalities of sensation in a partial distribution. Parietal lesions of different topography are responsible for this clinical picture, which probably represents a minor variant of the two previous sensory syndromes. Neuropsychological dysfunction was present in 17 patients. The only constant association was between conduction aphasia and right-sided pseudothalamic sensory deficit. We conclude that parietal stroke can cause different sensory syndromes depending on the topography of the underlying lesion. Sensory deficits can be monosymptomatic but never present as a "pure sensory stroke" involving face, arm, leg, and trunk together.

Opercular cheiro-oral syndrome.

Perioral and distal upper limb sensory dysfunction (cheiro-oral syndrome) has classically been attributed to cortical involvement. In previously reported cases of the syndrome, caused by stroke, however, the thalamus or brain stem has been the actual site of the lesion. We have studied two patients with infarct in the superficial middle cerebral artery territory involving the parietal operculum. Sensory involvement was purely subjective in the face, but severe hypoesthesia was present in the distal upper limb, involving mainly position sense, stereognosis, and graphesthesia. Temperature and pain sensation were involved in one patient. These findings correlated with involvement of the lower part of the postcentral gyrus, more caudal parts of the parietal operculum, and underlying white matter. This opercular cheiro-oral syndrome seems more uncommon than faciobrachiocrural hemihypesthesia associated with anterior parietal artery territory infarct. A double supply to the parietal opercular region through branches of the temporal arteries and anterior parietal artery may explain the rarity of cheiro-oral syndrome resulting from hemisphere stroke, because simultaneous and partial compromise to two different pial artery networks is uncommon.

Loss of psychic self-activation with bithalamic infarction. Neurobehavioural, CT, MRI and SPECT correlates.

Two patients with bilateral thalamo-mesencephalic infarct in the paramedian territory developed vertical gaze dysfunction and marked behavioural changes, in the absence of significant motor inability and formal neuropsychological impairment. While they were physically and emotionally active before stroke, they became apathetic, aspontaneous, indifferent, and seemed to have lost motor and affectic drive, as well as the need itself for any psychic activity. However, this mental and motor inertia was reversible when the patients were repeatedly stimulated by another person. This need for constant external programming, together with a lack of emotional reactivity, made the patients resemble robots. CT and MRI suggested involvement of the dorsomedial and midline nuclei of the thalamus, and SPECT showed remote frontomesial hypoperfusion. A disturbance of the striatal-ventral pallidal-thalamic-frontomesial limbic loop is suggested by previous reports of a similar "loss of psychic self-activation", "pure psychic akinesia", or "athymhormia" with bipallidal, bistriatal, or subcortical bifrontal lesions.

Double-blind study of nimodipine in non-severe stroke.

We evaluated the effect of nimodipine (30 mg q.i.d. orally for 14 days) on acute ischemic stroke of mild or moderate severity in a unicenter, double-blind, randomized, placebo-controlled pilot study. Treatment had to be started after CT, within 48 h of infarct in patients with a Mathew scale sum score between 50 and 75. The duration of follow-up was 4 months. Eight of the 60 randomized patients were excluded because of incorrect diagnosis. For the remaining 52 patients, 24 were allocated to nimodipine and 28 to placebo. Analysis of variance and covariance and repeated measurements of the Mathew scale scores showed no difference between the two groups, who had continuous and parallel improvement. There was no recurrent stroke, but 1 control died 4 weeks after stroke. Treatment with nimodipine was well tolerated (hypotension: 1 treated patient, 3 controls; bradycardia: 1 treated patient, 2 controls; sGPT increase: 1 treated patient, 1 control). The lack of efficacy of nimodipine in this study may be due to: (1) the neurologic deficit not being severe enough, or (2) the delay before treatment was too long.

[Muscular diseases in relation to drug consumption]. / Les atteintes musculaires en relation avec la prise de médicaments.

Toxic myopathies are an uncommon manifestation of chemotherapeutic agents. Most myopathies are characterized by a weakness affecting proximal limb-muscles more than distal ones. Steroids, chloroquine and ipecac syrup are the most common drugs inducing myopathies. Toxic myositis is rare and reported with D-penicillamine abuse. Myotoxicity of local agents injection such as anesthetics, steroids or antibiotics is also known. Congenital myopathies such as malignant hyperthermia, hypokalemic periodic paralysis or paroxysmal myoglobinuria may also be induced by drugs but are very rare.

Thalamic infarcts: clinical syndromes, etiology, and prognosis.

We studied forty patients with CT-proven thalamic infarcts without involvement of the superficial territory of the posterior cerebral artery. The delineation into four arterial thalamic territories (inferolateral, tuberothalamic, posterior choroidal, paramedian) corresponded clinically to four different syndromes. The most common etiologies were lacunar infarction, large artery atherosclerosis with presumed artery-to-artery embolism, cardioembolism, and migrainous stroke. We found no risk factor other than age or oral contraceptive use in six patients. One patient died in the acute phase. During follow-up (45.6 months), the stroke or death rate was 7.4% per year. Delayed pain developed in three patients and abnormal movements in three. Late disability was mainly secondary to persisting neuropsychological dysfunction (thalamic dementia).

Ischemic stroke as the presenting manifestation of localized systemic cancer.

A cerebral infarct due to a thrombosis of the left pericallosal artery was the first manifestation of an ovarian adenocarcinoma in a 42-year-old woman. A paraneoplastic origin was suggested by the observation that this patient had chronic intravenous coagulation and subsequently developed migratory thrombophlebitis (Trousseau's syndrome) despite high dose vitamin K antagonists therapy. This was supported by the fact that all manifestations of the hypercoagulable state disappeared following surgical cure of the cancer. Because cerebral infarction can be the first manifestation of a potentially curable cancer, patients with a cerebral infarct of an unknown etiology should be investigated for a malignant process, if there is laboratory or clinical evidence od disseminated intravascular coagulation.

Transient global amnesia and stroke.

Four patients who experienced isolated transient global amnesia had computed tomographic evidence for a cerebral infarct (3 cases) or hemorrhage (1 case). The medial part of the temporal lobe was involved in 2 patients (left in 1, right in 1), the left lentiform nucleus in 1 patient, and the left thalamus in 1 left-handed patient. These findings suggest that transient global amnesia may be associated with stroke in some cases, but it has no localizing value within the temporodiencephalic structures. No cerebrovascular events occurred over a 1-to 5-year follow-up, suggesting that transient global amnesia with infarction or hemorrhage is not a strong predictor of further stroke.

Manic delirium and frontal-like syndrome with paramedian infarction of the right thalamus.

A disinhibition syndrome affecting speech (with logorrhoea, delirium, jokes, laughs, inappropriate comments, extraordinary confabulations), was the main manifestation of a right-sided thalamic infarct involving the dorsomedian nucleus, intralaminar nuclei and medial part of the ventral lateral nucleus. Resolution of conflicting tasks was severely impaired, suggesting frontal lobe dysfunction. These abnormalities correlated with the finding on SPECT of a marked hypoperfusion in the overlying hemisphere predominating in the frontal region. We suggest that this behavioural syndrome was produced by disconnecting the dorsomedian nucleus from the frontal lobe and limbic system.

Unilateral left paramedian infarction of thalamus and midbrain: a clinico-pathological study.

In a patient with a unilateral embolic infarct in the left posterior thalamo-subthalamic paramedian artery territory, neuropathological studies showed involvement of the intralaminar, dorsomedial, and internal part of the ventral posterior nuclei of the thalamus, of the rostral part of the mesencephalic reticular formation, and of the posterior commissure. The patient showed upgaze palsy for voluntary saccades, smooth pursuit and vestibulo-ocular movements, sustained downgaze, right-sided motor hemineglect and facio-brachial hypaesthesia, motor transcortical aphasia and anterograde amnesia. This case confirms that unilateral destruction of the posterior commissure, rostral interstitial nucleus of the MLF and interstitial nucleus of Cajal produces a non-dissociated upgaze palsy. Involvement of the nucleus of Cajal probably produced the sustained downward deviation of the eye, by causing predominance of downward vestibulo-ocular inputs. This case also shows that thalamic aphasia and anterograde amnesia may be related to a paramedian lesion of the thalamus, with special reference to involvement of the dorsomedial nucleus, in the absence of lesion of the pulvinar and mamillo-thalamic tract and of conspicuous involvement of the ventral lateral nucleus. Selective hemineglect for motor tasks may occur in infarction of the dominant thalamus, involving the intralaminar nuclei.

The syndrome of unilateral tuberothalamic artery territory infarction.

The study of 3 personal cases and 5 published cases of unilateral infarct limited to the territory of the tuberothalamic artery suggests that this syndrome should be differentiated from the other thalamic syndromes. The onset is usually sudden, with moderate contralateral weakness. Sensory changes may be present but remain mild. The patients are apathetic, show perseveration and may be disoriented. In left-sided infarcts, transcortical aphasia, verbal and visual memory impairment and sometimes acalculia are found. In right-sided infarcts, hemispatial neglect, visual memory impairment and disturbed visuospatial processing are common. A decreased level of consciousness, disturbed ocular movements, severe motor weakness and delayed abnormal movements do not occur. Involvement of the ventral lateral and dorsomedial nucleus with sparing of the intralaminar nuclei, posterolateral formation and upper midbrain may explain this picture. The fact that the tuberothalamic artery arises from the posterior communicating artery, which often receives its supply from the carotid system, further justifies considering unilateral tuberothalamic infarcts as a syndrome.

[Hemiataxia and ipsilateral sensory deficit. Infarct in the area of the anterior choroidal artery. Crossed cerebellar diaschisis]. / Hémiataxie et déficit sensitif ipsilatéral. Infarctus du territoire de l'artère choroïdienne antérieure. Diaschisis cérébelleux croisé.

A 58 year old hypertensive man suffered an acute right-sided hemiataxia associated with painful hypoesthesia. CT showed an infarct in the territory of the left anterior choroidal artery. The sensory defect involved all the elementary modes, but predominated on pain sensation. The ataxia suggested a cerebellar type of dysfunction, with hypermetria, intentional tremor, dysdiadochokinesia and a positive rebound phenomenon. There was no hemiparesis, no hemianopia, no neuropsychological dysfunction and no oculomotor abnormality. Hemiataxia with hemisensory defect has not been reported in stroke, and it constitutes a new clinical form of lacunar syndrome. The hemiataxia may be related to the finding on single-photon emission computed tomography (SPECT) using 123 I-amphetamine of a crossed cerebellar diaschisis, which may suggest a transneuronal deactivation. This metabolic depression may have been due to involvement of the temporo-parieto-pontine bundle of Türck in the retro and sub-lenticular portion of the internal capsule. The finding of a normal cortical blood flow may explain why no neuropsychological impairment was present, because of the absence of functional deactivation of the cortex by the underlying deep infarct.

Painful ataxic hemiparesis.

Right hemiparesis with right-sided pain and ataxia developed in a 68-year-old man. Sensation, neuropsychological function, and somatosensory evoked potentials were normal. Computed tomography showed an isolated fresh infarct in the left part of the thalamus. The pain and ataxic disturbances were related to involvement of the thalamus itself, but the hemiparesis with hyperactive tendon reflexes and Babinski's sign was probably due to associated dysfunction in the adjacent internal capsule from compression or edema. In the available clinicopathological reports of cases with hemiparesis and thalamic infarction, contiguous involvement of the internal capsule or no associated lesion has been reported. Because of the occurrence of pain, which is not present in pontine, mesencephalic, or capsular ataxic hemiparesis, we suggest that the syndrome seen in our patient be called "painful ataxic hemiparesis."

[Staged or bilateral malacias in the area of the middle cerebral or posterior cerebral arteries. Comparative study of the risk of multifocal stroke in 120 patients]. / Les ramollissements étagés ou bilatéraux du territoire des artères cérébrales moyennes ou cérébrales postérieures. Etude comparative du risque d'atteinte multifocale chez 120 patients.

We studied and compared 120 cases with an infarction in the superficial area of the middle cerebral artery (MCA) or the posterior cerebral artery (PCA). Among the patients with an infarction of the MCA area, 8% had a capsular involvement and 3% a delayed contralateral sylvian infarction. Among the patients with an infarction of the PCA area, 35% had a thalamo-mesencephalic involvement and 23% a delayed contralateral occipital infarction. Thus, multifocal infarction was significantly more frequent in the PCA area than in the MCA area. No particular vascular risk factor could explain this difference, which may be related to general constitutional factors, such as the type of collateral supply or the vascular anatomy itself. In the PCA area only, we found a significant association between the severity of risk factors and occurrence of multifocal infarction.

Upgaze palsy and monocular paresis of downward gaze from ipsilateral thalamo-mesencephalic infarction: a vertical "one-and-a-half" syndrome.

A patient with an infarct limited to the paramedian thalamus and upper mesencephalon on the right side suffered a conjugate upgaze palsy associated with a monocular paresis of downward gaze in the ipsilateral eye (vertical "one-and-a-half" syndrome). This paresis involved tonic and phasic components. Vertical oculocephalic movements and conjugate horizontal gaze were normal. It is suggested that the unilateral lesion destroyed the fibres of the posterior commissure and the descending fibres to the ipsilateral subnucleus of the inferior rectus and contralateral subnucleus of the superior oblique just after they decussate, probably above the level of the third nerve nucleus. A complex disturbance of vertical gaze may be due to a unilateral thalamo-mesencephalic lesion.

The response of focal ischemic cerebral edema to dexamethasone.

Twenty-four h after permanent occlusion of the middle cerebral artery (MCA) in the cat, the hemispheric swelling due to edema is markedly reduced under treatment with large doses of dexamethasone than is the case with the untreated group. The increase of regional water and sodium content in the MCA territory is less in the dexamethasone treated group, whereas the potassium changes in the ischemic tissue showed only small differences between the two groups. The potassium content of the non-ischemic tissue is slightly increased in the dexamethasone treated animals when comparing with the untreated group. RISA activity in the tissue is increased in the grey and the white matter of both groups. The less marked RISA-131 activity in the cortical grey matter of the treated animals indicates blood-brain barrier damage of a smaller degree due to dexamethasone. These findings indicate a beneficial effect of dexamethasone on local ischemic edema. Regarding our results and the pharmacokinetics of this steroid the dexamethasone loading of a patient has to be in the range of about 100 mg per day for the adult, and has to be started immediately after the onset of a stroke.