Aphasic-type language disorders associated with lesions of the putamen and caudate nucleus: clinicopathological findings in one case (author's transl)

Language disorders developed in a patient following a subcortical infarct involving the left putamen and caudate nucleus. Language was abundant and fluent, with many perseverations, semantic and ideation incoherences, and all activities concerned with verbal or non-verbal expression were affected. Lesions were present in the head and body of the caudate nucleus, the whole of the putamen, the anterior nucleus of the thalamus and the superior part of the internal capsule. The disorder was unique in relation to disturbances of the aphasic type observed in extensive thalamic lesions, or in transcortical sensorial aphasia. Physiopathological interpretation is based on the functional role of the putamen-caudate system in the regulation of many types of behaviour: animal experiments and results of applying stimuli in humans suggests a release of the inhibition exerted by the caudate nucleus on the frontal cortex. Lack of comparable clinicopathological data implies that other similar cases must be reported before the specificity of the disorder can be confirmed.     

A case of left thalamic infarction with aphasia and dysgraphia in Kanji]

We reported an 11-year-old girl with left thalamic infarction causing aphasia and dysgraphia. The lesion corresponded to the perfusion area of the tuberothalamic and paramedian arteries. Confrontation naming and word finding were impaired, but phonological cuing was very helpful despite the absence of amnesia. Dysgraphia was observed only in Kanji (morphogram) writing, and was also improved by visual cuings. These findings suggested difficulty in memory retrieval, in which the left thalamus might have some role.     

A case of crossed aphasia with apraxia of speech

Apraxia of speech (AOS) is a rare, but well-defined motor speech disorder. It is characterized by irregular articulatory errors, attempts of self-correction and persistent prosodic abnormalities. Similar to aphasia, AOS is also localized to the dominant cerebral hemisphere. We report a case of Crossed Aphasia with AOS in a 48-year-old right-handed man due to an ischemic infarct in right cerebral hemisphere.     

Motor speech disorders associated with primary progressive aphasia

Background: Primary progressive aphasia (PPA) and conditions that overlap with it can be accompanied by motor speech disorders. Recognition and understanding of motor speech disorders can contribute to a fuller clinical understanding of PPA and its management as well as its localisation and underlying pathology.

Aims: To review the types of motor speech disorders that may occur with PPA, its primary variants, and its overlap syndromes (progressive supranuclear palsy syndrome, corticobasal syndrome, motor neuron disease), as well as with primary progressive apraxia of speech.

Main Contribution: The review should assist clinicians’ and researchers’ understanding of the relationship between motor speech disorders and PPA and its major variants. It also highlights the importance of recognising neurodegenerative apraxia of speech as a condition that can occur with little or no evidence of aphasia.

Conclusion: Motor speech disorders can occur with PPA. Their recognition can contribute to clinical diagnosis and management of PPA and to understanding and predicting the localisation and pathology associated with PPA variants and conditions that can overlap with them.     

A case of Foix-Chavany-Marie syndrome and crossed aphasia after right corona radiata infarction with history of left hemispheric infarction]

Foix-Chavany-Marie syndrome (FCMS) is a syndrome that presents facio-pharyngo-glosso-masticatory diplegia with automatic voluntary dissociation. Its most common etiology is stroke in the regions of bilateral opercula. We described a 75-year-old woman with FCMS and crossed aphasia. She had cerebral infarction of left middle cerebral artery territory 23 years before. At that time she had transient right hemiparesis, but no aphasia. This time, she suddenly became mute and was brought to our hospital. Neurological examination revealed severe weakness in her bilateral lower face, pharynx, tongue, and sternocleidomastoideus. She had no weakness of limbs. Her listening comprehension was moderately disturbed and handwriting was paragraphic. Her emotional facial movement was maintained despite of disturbed volitional facial movement. CT scan disclosed fresh infarction at the right corona radiata and old infarction at the left middle cerebral artery territory. In this patient, lesions at the left operculum and right corona radiata with the preserved right operculum gave rise to FCMS. This implies following possibilities: 1) the corticobulbar tract and corticospinal tract run separately at the corona radiata, 2) volitional and emotional tracts of facial movement run separately at the corona radiata. It was demonstrated that FCMS is not always caused by bilateral operculum lesions. Our patient did not show aphasia after the first stroke including left language area, but became severely aphasic after the right corona radiata infarction. Simultaneous occurrence of FCMS and aphasia after corona radiata lesion suggested that the corticobulbar tract and a tract that conducts linguistic information are running adjacently in the corona radiata. Our case suggested that restricted corona radiata lesion may cause severe subcortical aphasia and in case of additional contralateral corticobulbar tract lesion, severe dysarthria may occur.     

A case of conduction aphasia due to small infarction in the left parietal lobe]

This is a report on the patient with conduction aphAsia due to small infarction in the left parietal lobe. The patient is a right-handed man aged 74, who developed a speech disorder and mild paralysis of the right hand on November 13. 1996. A CT scan showed a small low-density in the supramarginal gyrus of the left parietal lobe. Standard Language Test of aphasia (SLTA) conducted at five days after admission to the hospital showed preserved auditory comprehension and phonemic para-aphasia symptoms with respect to volitional speech, naming, reading aloud and repetition. Frequent self-correction was also observed while repetition was not remarkably impaired. A test at three months after the onset revealed generally fluent speech, while there still remained occasional phonemic para-aphasia and self-correction for the speech disruption. Three years and four months later, most of the aphasic syndromes disappeared, although the patient claimed he still had difficulty in speaking. This case suggests that conduction aphasia can be caused by a lesion, though small, located in arcuate fibers of the cerebrum. The characteristics are phonemic para-aphasia with respect to general speech functions as well as self-correction toward target words. The indicated that lesions in the pathway connecting Broca's area and Wernicke's area causes difficulties in selecting accurate phonemes due to a malfunctioning interface between the two areas.     

A case of progressive apraxia of speech and non-fluent aphasia

Abstract

A 67-year-old female presented with a progressive deficit over a 2–2 1/2-year period characterized by apraxia of speech and mild non-fluent aphasia. Mild neuropsychological impairments were incompatible with the typical clinical syndrome of dementia. Mild right upper extremity motor impairment and SPECT findings were localizable to the left hemisphere. There was no identifiable cause for the progressive deficits in motor speech and expressive language. The patient's deficit appears to represent a variant of the recently described clinical presentation of progressive motor speech compromise.     

A new enzyme marker for striatal compartmentalization: NADPH diaphorase activity in the caudate nucleus and putamen of the cat

The distribution of dihydronicotinamide adenine dinucleotide phosphate diaphorase (NADPH diaphorase) was studied by enzyme histochemistry in the striatum of the adult cat. Neurons and neuropil expressing NADPH diaphorase activity were found throughout the striatum. The diaphorase-positive neurons formed a sparse population of medium-sized cells. In the caudate nucleus they were recognized by antisera against somatostatin 14, somatostatin 28(1-12), neuropeptide Y and avian pancreatic polypeptide. The diaphorase activity of the striatal neuropil was characterized by a modular organization that was particularly distinct in the caudate nucleus. This organization was analyzed by comparing the patterns of diaphorase staining with the distribution of acetylcholinesterase activity in adjacent sections. The NADPH diaphorase activity was found to be dense in the acetylcholinesterase-rich matrix of the caudate nucleus, but weak in the acetylcholinesterase-poor compartments known as striosomes. Because of the colocalization of perikaryal NADPH diaphorase activity and somatostatinlike immunoreactivity, a comparison was also made between the distribution of diaphorase staining and immunostaining for somatostatinlike peptide in the striatal neuropil. Both observed striosomal ordering, so that the acetylcholinesterase-poor zones detected in adjoining sections corresponded to regions of low somatostatinlike immunoreactivity as well as low NADPH diaphorase staining. In some regions striosomes were more clearly delineated in the stains for diaphorase and somatostatinlike suggest that NADPH diaphorase may be a sensitive marker for the somatostatinergic neuropil as well as the somatostatinergic perikarya of the striatum, and that this enzyme could prove valuable in attempts to differentiate the processes of intrinsic somatostatin-containing fibers from any extrinsic somatostatin afferents that may exist.     

In vivo release of endogenous dopamine from rat caudate putamen and nucleus accumbens by 40 mM potassium chloride

1. 1. The resting and K⁺-stimulated release rates of endogenous dopamine (DA) have been measured in vivo at four different sites in the rat caudate putamen and nucleus accumbens.

2. 2. A push-pull cannula was inserted into the brain sites chosen, and the tissue was perfused with artificial cerebrospinal fluid (CSF) containing 2.6 or 40 mM KC1. The DA content of the perfusates was determined by a radioenzymatic procedure.

3. 3. DA release was significantly increased above unstimulated levels by 40 nM KC1 in all areas tested. Neither unstimulated nor K⁺-stimulated release rates varied significantly among the regions examined.

4. 4. K⁺-stimulated DA release was not significantly diminished by perfusing the tissue with calcium-free medium, suggesting that release was probably supported by residual amounts of calcium in the tissue.

A case of aphasia following left thalamic hemorrhage

In a patient without fluent speech, good comprehension, aphasia and frequent neologisms, computerized tomography (CT scan) demonstrated a left posterior thalamic hemorrhage sparing other language areas. We discuss the existence and the anatomical and pathogenetic mechanisms of thalamic aphasia.     

Symptomatic hemidystonia of delayed onset. Magnetic resonance demonstration of pathology in the putamen and the caudate nucleus

We present a case of symptomatic hemidystonia of delayed onset. The primary disease was a perinatal, presumed cerebrovascular infarction brought about by febrile illness with convulsions 12 weeks after partus. After many years without neurological symptoms, the hemidystonia started in adolescence, and became stationary after 4 years of mild progression. Magnetic resonance imaging revealed atrophy of the right striatum including the caudate nucleus and putamen. The symptoms responded moderately to treatment with benzhexol.     

Quantitative morphology of the caudate and putamen in patients with cocaine dependence

OBJECTIVE: Deficits in dopaminergic function may contribute to hypertrophy of striatal structures associated with typical neuroleptic treatment. In light of a body of research that has associated chronic cocaine use with extrapyramidal symptoms and striatal dopaminergic depletion, the authors looked for evidence of striatal dysmorphology in patients with chronic cocaine dependence. METHOD: Caudate, putamen, and total brain volumes were quantified by means of magnetic resonance imaging in 25 cocaine-dependent and 20 healthy subjects. RESULTS: Normalized caudate and putamen volumes were 3.40% and 9.18% larger, respectively, in the cocaine-dependent subjects. CONCLUSIONS: These observations suggest that deficits in dopaminergic function associated with cocaine dependence may contribute to striatal hypertrophy.     

Muscarinic cholinergic receptor binding and electrophysiological response to acetylcholine in cultured rat caudate putamen nucleus neurons

Binding sites with specificity for N-[3H]methylscopolamine ([3H]NMS) are present in homogenates of primary culture neurons from the rat caudate putamen nucleus (CPN). Specific binding is saturable with respect to [3H]NMS. The Scatchard analysis indicates a dissociation constant of 0.6 nM and a density of 7.0 X 10(3) per cell, or 78 fmol/mg protein. In electrophysiological measurements, excitatory postsynaptic currents (EPSCs) in larger cells were increased by pressure application of acetylcholine under voltage clamp condition. The EPSCs may come from neighboring smaller cells with muscarinic acetylcholine receptors.     

电刺激大鼠右侧尾壳核诱导皮层脑电高频振荡的特征

目的 探讨电刺激大鼠右侧尾壳核诱导皮层脑电高频振荡(HFO)功率谱特征.方法 实验共用雄性SD大鼠56只,体质量150?250 g,氨基甲酸乙酯麻醉下行气管插管和开颅术.将一根双极不锈钢同芯刺激电极植于右侧尾壳核,重复施加电刺激(60 Hz,2 s,0.4?0.6 mA);将两个不锈钢螺丝钉旋入双侧皮层的颅骨内,一个不...     

Dopamine D2 and D3 receptors in human putamen, caudate nucleus, and globus pallidus

Because radioactive raclopride and radioactive (+)-4-propyl-9-hydroxynaphthoxazine ((+)-PHNO) are used to image dopamine (DA) D2 and D3 receptors in the striatum and globus pallidus in humans, the present study examined the proportions of D2 and D3 receptors in postmortem tissues from these regions. Conflicting results were obtained when using a single concentration of remoxipride to occlude D2 receptors or using a single concentration of U99194A or FAUC 365 to occlude D3 receptors. However, using a range of concentrations of FAUC 365, a D3-selective antagonist, to inhibit the binding [(3)H]raclopride or [(3)H]-(+)-PHNO to D3 receptors at low concentrations (1-10 nM) and to inhibit ligand binding to D2 receptors at higher concentrations (100-2000 nM), it was possible to measure the proportion of D2 and D3 receptors in the tissues. This method revealed that these two radioligands detected only D2 receptors in the dorsal putamen and the dorsal caudate nucleus, but detected a mixed population of two-thirds D2 and one-third D3 DA receptors in the ventral putamen, the ventral caudate, and the globus pallidus. The present findings are in good agreement with the known gene expression data for D2 and D3 receptors in these human brain regions.     

An autopsy case of caudate nucleus lobulation accompanied with diaphragmatic eventration

We describe an autopsy female case of multiple anomalies with lobulation of caudate nucleus tail, diaphragmatic eventration, skeletal anomalies, pyramidal tract anomaly, and meningothelial meningioma. Her psychomotor development was delayed, and she developed bilateral eventration of the diaphragms on X-ray film in her third decades. Right hemi-colonectomy was performed for volvulus at the age of 44 years, and meningioma was incidentally identified. She died at the age of 47 years. Autopsy demonstrated the partial deficiency of the muscular tissue in the circular thinned membranous area predominantly on left side including the central tendon of the diaphragm. The tails of the bilateral caudate nucleus demonstrated excessive lobulations, and the brainstem pyramidal tract showed hypoplasia. Immunoreactivity for tyrosine hydroxylase was deficient in the lobulated tail of caudate. We believe that this case is characterized by a rare combination of eventration, skeletal and nervous anomalies.