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PubMed2001

The place of the thalamus in frontal cortical-basal ganglia circuits.

The thalamus has long been thought to convey subcortical information to the cortex. Indeed, models of basal ganglia function attribute the primary role for the thalamus to a simple relay of information processed in the basal ganglia to the cortex. The thalamic nuclear groups that are associated primarily with this function are the ventral anterior and ventral lateral nuclei and the mediodorsal thalamic nucleus. However, recent studies have shown that the corticothalamic projection is important for the dynamics of the thalamocortical processing. Furthermore, the relay nuclei that carry basal ganglia output to the cortex have recently been shown to project back to the basal ganglia directly. These two recent developments indicate a more dynamic role for the thalamus in basal ganglia information processing than a passive relay.

Animals↗

PubMed2000

The indirect basal ganglia pathway in dopamine D(2) receptor-deficient mice.

Recent pathophysiological models of basal ganglia function in Parkinson's disease predict that specific neurochemical changes in the indirect pathway would follow the lack of stimulation of D(2) dopamine receptors. Post mortem studies of the basal ganglia in genetically modified mice lacking functional copies of the D(2) dopamine receptor gene allowed us to test these predictions. When compared with their congenic N(5) wild-type siblings, mice lacking D(2) receptors show an increased expression of enkephalin messenger RNA in the striatum, and an increased activity and expression of cytochrome oxidase I in the subthalamic nucleus, as expected. In addition, D(2) receptor-deficient mice display a reduced expression of glutamate decarboxylase-67 messenger RNA in the globus pallidus, as the basal ganglia model predicts. This reduction contrasts with the lack of change or increase in glutamate decarboxylase-67 messenger RNA expression found in animals depleted of dopamine after lesions of the mesostriatal dopaminergic system. Furthermore, D(2) receptor-deficient mice show a significant decrease in substance P messenger RNA expression in the striatonigral neurons which form the direct pathway. Finally, glutamate decarboxylase-67 messenger RNA expression in the basal ganglia output nuclei was not affected by mutations in the D(2) receptor gene, a fact that could probably be related to the absence of a parkinsonian locomotor phenotype in D(2) receptor-deficient mice. In summary, these findings provide compelling evidence demonstrating that the lack of endogenous stimulation of D(2) receptors is sufficient to produce subthalamic nucleus hyperactivity, as assessed by cytochrome oxidase I histochemistry and messenger RNA expression, and strongly suggest the existence of interactions between the basal ganglia direct and indirect pathways.

Animals↗

PubMed2005

The clinico-radiologic properties of deep small basal ganglia infarction: lacune or small striatocapsular infarction?

OBJECTIVE: Deep small basal ganglia infarction (DSBI) cannot be clearly classified as either lacune or striatocapsular infarction by their sizes only. We tried to elucidate clinical and other properties of DSBI to understand better in pathophysiology of ischemic lesion of basal ganglia. METHODS: We analyzed 36 patients with acute ischemic lesion of basal ganglia with the size varying from 1.5 to 3 cm in maximal diameters. We assessed clinical features, laboratory data, risk factors of stroke, and radiologic findings such as MRI and MR angiography. RESULTS: Patients with DSBI could be largely divided into two distinctive groups, small infarction with cortical sign (SICS) and lacunar syndrome (LS) according to their presence of cortical manifestations. Total of 11 patients were in SICS group and they showed cortical manifestations such as eyeball deviation, visual field defect, aphasia and neglect. They also showed severer non-cortical neurologic deficit compared with LS group. Whereas LS group showed various MRA patterns, 7 patients of SICS group (63.6%) showed proximal MCA stenosis in MRA. CONCLUSIONS: We found that many patients with DSBI could have the features of either lacune or striatocapsular infarction. Although they have similar morphologic characteristics but they are presumed to have different pathophysiologic mechanism.

Adult↗

PubMed2006

[Basal ganglia calcification: clinical manifestations and diagnostic evaluation].

Physiological intracranial calcification occurs in about 0,3-1,5% of cases. It is asymptomatic and is detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases and other. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Such parkinsonism doesn't respond to drugs containing levodopha. Infections (toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders (blood calcium level and other), those are: Cockayne syndrome, tuberous sclerosis, Fahr's syndrome, Down syndrome and other. We observed some cases of basal ganglia calcification and studied clinical manifestations and treatment tolerance of this pathological condition. Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, serum concentration of calcium, phosphorus, and parathyreoid hormone is suggested to be determined in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism. Basal ganglia calcification in young patient with acute hepatitis may be result of Wilson disease.

Adolescent↗

PubMed1990

Germ cell tumors of the thalamus and the basal ganglia.

Two cases of germ cell tumors (GCTs) of the basal ganglia are presented and 40 previously reported cases are reviewed. The incidence of GCTs of the basal ganglia and thalamus was estimated as less than 14% of all intracranial GCTs. All patients except for two (95%) were male, aged 7-19 years. The clinical course was usually slow. The major symptoms were hemiparesis, mental deterioration such as dementia or character change, precocious puberty, diabetes insipidus, oculomotor palsy, speech disturbance, and hemianopsia. Signs of intracranial hypertension did not occur until the late stages of the disease. The plain CT finding was characterized by an irregularly defined, slightly high-density area frequently accompanied by central low-density areas without significant mass effect. The tumors showed mild to moderate and nonhomogeneous contrast enhancement. An ipsilateral cerebral hemiatrophy was often found. MR images demonstrated the corresponding findings. GCTs of the basal ganglia had a high possibility of containing components other than germinoma such as choriocarcinoma, endodermal sinus tumor, and embryonal carcinoma. Thus, tumor markers in the serum, CSF, or cyst fluid were frequently positive. With recent refinement of microsurgical techniques as well as immunohistochemical study and measurements of tumor markers of serum, CSF, and cyst fluid, major resections of tumor, accurate pretreatment histologic diagnosis, and early determination of the specific types of this tumor appear to be readily possible. This is essential for effective treatment of patients not only with radiosensitive germinoma, but also those with radioinsensitive nongerminoma variants and a combination of them located in this region.

Adolescent↗

PubMedDate not supplied

Relationship between obsessive-compulsive disorders and diseases affecting primarily the basal ganglia.

Obsessive-compulsive disorder (OCD) has been reported in association with some neurological diseases that affect the basal ganglia such as Tourette's syndrome, Sydenham's chorea, Parkinson's disease, and Huntington's disease. Furthermore, studies such as neuroimaging, suggest a role of the basal ganglia in the pathophysiology of OCD. The aim of this paper is to describe the association of OCD and several neurologic disorders affecting the basal ganglia, report the existing evidences of the role of the basal ganglia in the pathophysiology of OCD, and analyze the mechanisms probably involved in this pathophysiology.

Basal Ganglia↗

PubMed2000

Motor and non-motor sequence learning in patients with basal ganglia lesions: the case of serial reaction time (SRT).

In order to address the question of whether the basal ganglia are involved exclusively in regulation of motor sequence learning, or if they are involved in non-motor sequence learning as well, two versions of the serial reaction time (SRT) task were administered: First is the standard version of the SRT task in which the sequence is executed motorically, and the second is a non-motor version of the task which requires response only to a particular position of the sequence. Sixteen patients with damage restricted to the region of the basal ganglia and 16 matched control subjects participated in this study. In addition to the motor and non-motor SRT tasks, two declarative memory tests (Visual Paired Associates and Rey Auditory-Verbal Learning Test) were administered to the participants. Results indicate that the two groups did not differ either on learning rate of the two declarative tasks, or on the declarative component of the SRT tasks (i.e., 'generate'). However, the control group was significantly superior to the basal ganglia (BG) group in learning a specific sequence in the motor and non-motor SRT tasks. Results suggest that the basal ganglia are involved in the regulation of non- motor as well as motor sequence learning.

Adult↗

PubMed1987

Stereotactic resection of juvenile pilocytic astrocytomas of the thalamus and basal ganglia.

Six patients with juvenile pilocytic astrocytomas of the thalamus or basal ganglia underwent seven computer-assisted stereotactic laser craniotomies with complete or nearly complete removal of the tumor in all cases. The tumor was located in the right basal ganglia in one patient, the left basal ganglia in one patient, and the left thalamus in four patients. Postoperative assessment of the completeness of tumor removal was confirmed by contrast-enhanced computed tomographic scanning within the first 2 weeks after operation. None of the patients was neurologically worse after the procedure, and five were improved. The duration of follow-up ranged from 6 months to 3.5 years. In this group of patients, the computer-assisted, stereotactically guided resection of these deeply located, benign tumors was accomplished with no morbidity or mortality.

Adolescent↗

PubMed2002

Seizures and the basal ganglia: a review of the clinical data.

This article attempts an overview of the clinical and electrophysiological evidence supporting the involvement of the basal ganglia in epileptic seizures. In contrast to animal data, evidence for a role of these structures in human epilepsies is lacking. However, from the theoretical point of view, it remains conceivable that, given their strong interconnectivity, basal ganglia could be functionally linked to the cerebral cortex during an epileptic seizure. Several clinical ictal aspects have been suggested to be compatible with the involvement of basal ganglia, namely, ictal dystonic posturing during temporal lobe seizures, rotatory seizures and paroxysmal dyskinesia-like seizures. On the other hand, basal ganglia dysfunction may also influence some aspects of epilepsy, as suggested by pure basal ganglia pathology such as Parkinson's disease, or the described effect of an acute basal ganglia lesion in epileptic patients. The data discussed in this review may stimulate further research to link basic scientific data to human epilepsies, and lead to the development of novel therapeutical solutions.

Animals↗

PubMed2004

Properties of dopamine release and uptake in the songbird basal ganglia.

Vocal learning in songbirds requires a basal ganglia circuit termed the anterior forebrain pathway (AFP). The AFP is not required for song production, and its role in song learning is not well understood. Like the mammalian striatum, the striatal component of the AFP, Area X, receives dense dopaminergic innervation from the midbrain. Since dopamine (DA) clearly plays a crucial role in basal ganglia-mediated motor control and learning in mammals, it seems likely that DA signaling contributes importantly to the functions of Area X as well. In this study, we used voltammetric methods to detect subsecond changes in extracellular DA concentration to gain better understanding of the properties and regulation of DA release and uptake in Area X. We electrically stimulated Ca(2+)- and action potential-dependent release of an electroactive substance in Area X brain slices and identified the substance as DA by the voltammetric waveform, electrode selectivity, and neurochemical and pharmacological evidence. As in the mammalian striatum, DA release in Area X is depressed by autoinhibition, and the lifetime of extracellular DA is strongly constrained by monoamine transporters. These results add to the known physiological similarities of the mammalian and songbird striatum and support further use of voltammetry in songbirds to investigate the role of basal ganglia DA in motor learning.

Animals↗

PubMed1990

The basal ganglia and the initiation of movement.

The positive and negative signs of basal ganglia disease provide strong clinical evidence that the basal ganglia and allied nuclei participate in the neural mechanisms underlying volitional activity. This chapter reviews the range of neural subsystems in the basal ganglia that may contribute to these functions and their relationships with the dopamine-containing cell groups of the substantia nigra.

Animals↗

PubMed2003

Inhibition of ongoing responses following frontal, nonfrontal, and basal ganglia lesions.

The authors investigated the role of the frontal lobes and the basal ganglia in the inhibition of ongoing responses. Seventeen patients with frontal lesions (FG), 20 patients with lesions outside the frontal cortex (NFG), 8 patients with lesions to the basal ganglia (BG), and 20 orthopedic controls (OG) performed the stop-signal task that allows the estimation of the time it takes to inhibit an ongoing reaction (stop signal reaction time [SSRT]). The FG and the BG showed significantly longer SSRTs than the OG. Within the FG, patients with right and bilateral lesions showed significantly longer SSRTs than patients with left lesions. Results provide evidence for a role of the frontal lobes and the basal ganglia in the inhibition of ongoing responses.

Adult↗

PubMed2002

Basal ganglia lesions in 'Pick complex': a topographic neuropathological study of 19 autopsy cases.

The distribution of basal ganglia lesions, including the amygdala, striatum (caudate nucleus, putamen), pallidum, and substantia nigra, were reinvestigated in 19 Japanese autopsy cases of 'Pick complex', consisting of five patients with corticobasal degeneration (CBD), 10 patients with Pick's disease with Pick bodies (PDPB), and four patients with generalized variant of Pick's disease (gvPD). The lesions in the amygdala, striatum, and pallidum were classified into three categories (severe, moderate, and slight). The lesions in the substantia nigra were qualitatively judged, compared with normal controls. In CBD, basal ganglia lesions in all five cases were uniform: the pallidum showed severe lesions, the striatum moderate lesions, the amygdala slight lesions, and obvious neuronal loss of the substantia nigra was verified in all five cases. Basal ganglia lesions in 10 cases of PDPB were also uniform: the amygdala disclosed severe to moderate lesions, the striatum moderate to slight lesions, the pallidum slight lesions, while obvious neuronal loss of the substantia nigra was found in only two of nine cases in which this structure was examined. Furthermore, basal ganglia lesions in all four cases of gvPD were uniform: the caudate nucleus showed severe lesions, the putamen and amygdala severe to moderate lesions, the pallidum moderate to slight lesions, and obvious neuronal loss of the substantia nigra was confirmed in all four cases. This study, using conventional staining such as hematoxylin-eosin and Holzer, clarified that there were prominent lesions in the pallidum in CBD, in the amygdala in PDPB, and in the caudate nucleus in gvPD, respectively. In addition, nigral involvement was usually found in CBD and gvPD, but was rarely seen in PDPB. These neuropathological findings may help to elucidate the pathological heterogeneity of basal ganglia lesions in 'Pick complex'.

Aged↗

PubMed2001

Basal ganglia dysfunction in Tourette's syndrome: a new hypothesis.

Tourette's syndrome is a neuropsychiatric syndrome with onset in childhood that is characterized by chronic multiple tics. The cause of Tourette's syndrome is unknown, but the pathophysiology most likely involves basal ganglia and frontocortical circuits. A useful scheme of basal ganglia dysfunction should be able to account for the features that make Tourette's syndrome unique, in addition to the features that Tourette's syndrome shares with other disorders. Recent advances in knowledge of basal ganglia functional anatomy and physiology make it possible to hypothesize how specific neural mechanisms relate to specific clinical manifestations of Tourette's syndrome. A model of selection and suppression of competing behaviors by the basal ganglia is presented. The functional anatomy of basal ganglia circuits and new information on dopamine modulation of those circuits provide the basis for hypotheses of basal ganglia dysfunction in Tourette's syndrome.

Basal Ganglia↗

PubMed2002

Hypothalamic digoxin related membrane Na+-K+ ATPase inhibition and familial basal ganglia calcification.

The isoprenoid pathway produces three key metabolites-digoxin (membrane sodium-potassium ATPase inhibitor and regulator of intracellular calcium-magnesium ratios), dolichol (regulator of N-glycosylation of proteins) and ubiquinone (free radical scavenger). The pathway was assessed in a rare and specific type of familial basal ganglia calcification described. The family had a coexistence of basal ganglia calcification (six out of 10 cases), schizophrenia, Parkinson's disease, Alzheimer's disease, rheumatoid arthritis, systemic tumours and syndrome X and were all right hemispheric dominant. The isoprenoid pathway was also studied for comparison in right hemispheric dominant, bihemispheric dominant and left hemispheric dominant individuals. The isoprenoid pathway was upregulated with increased digoxin synthesis in familial basal ganglia calcification. Membrane sodium-potassium ATPase inhibition can lead on to increase in intracellular calcium and calcification of the basal ganglia. There was increase in tryptophan catabolites and a reduction in tyrosine catabolites. There was also an increase in dolichol and glycoconjugate levels with reduced lysosomal stability in these patients. The ubiquinone levels were low and free radical levels increased. The cholesterol-phospholipid ratio was increased and glycoconjugate level of the RBC membrane reduced in these group of patients. No significance difference was noted in family members with and without basal ganglia calcification. This findings were correlated with the pathogenesis of syndrome X, immune mediated diseases, degenerations, tumours and psychiatric disorders noted in the familial basal ganglia calcification described. The biochemical patterns obtained in familial basal ganglia calcification correlated with those in right hemispheric dominance.

Adult↗

PubMed2002

The roles of the cerebellum and basal ganglia in timing and error prediction.

Recent evidence that the cerebellum and the basal ganglia are activated during the performance of cognitive and attention tasks challenges the prevailing view of their primary function in motor control. The specific roles of the basal ganglia and the cerebellum in cognition, however, have been difficult to identify. At least three functional hypotheses regarding their roles have been proposed. The first hypothesis suggests that their main function is to switch attentional set. The second hypothesis states that they provide error signals regarding stimuli or rewards. The third hypothesis is that they operate as an internal timing system, providing a precise representation of temporal information. Using functional magnetic resonance imaging, we tested these three hypotheses using a task-switching experiment with a 2 x 2 factorial design varying timing (random relative to fixed) and task order (unpredictable relative to predictable). This design allowed us to test whether switching between tasks, timing irregularity and/or task order unpredictability activate the basal ganglia and/or the cerebellum. We show that the cerebellum is primarily activated with timing irregularity while the anterior striatum is activated with task order unpredictability, supporting their distinctive roles in two forms of readjustment. Task order unpredictability alone, independent of reward delivery, is sufficient to induce striatal activation. In addition, activation of the cerebellum and basal ganglia were not specific to switching attention because these regions were both activated during switching between tasks and during the simultaneous maintenance of two tasks without switching between them.

Adaptation, Physiological↗

PubMed2006

Post-stroke affective or apathetic depression and lesion location: left frontal lobe and bilateral basal ganglia.

This study was designed to examine the correlation between damage to the basal ganglia or frontal lobe and depression status (both affective and apathetic dimensions) in 243 stroke patients. We assessed the affective dimension in post-stroke depression (PSD) using the Zung Self-rating Depression Scale (SDS) and the apathetic dimension in PSD using the apathy scale (AS). We classified basal ganglia or frontal lobe damage into four groups: no damage, damage to the left side only, damage to the right side only, and damage to both sides. Affective and/or apathetic PSD was found in 126 patients (51.9%). The severity of affective depression (SDS score) was associated with left frontal lobe (but not basal ganglia) damage, and that of apathetic depression (AS score) was related to damage to the bilateral basal ganglia (but not to the frontal lobe). The anatomical correlates of PSD differ depending on the PSD dimension (affective or apathetic) and may explain interstudy differences regarding the association between lesion location and type of PSD.

Aged↗

PubMed1994

Somatomotor and cardiorespiratory responses to basal ganglia stimulation in cats.

The electrical stimulation of the neural elements within the basal ganglia circuitry caused characteristic somatomotor activities and changes in arterial blood pressure (BP), heart rate (HR), and respiratory rate (RR) in conscious, unrestrained cats. A highly constant pattern of responses was elicited by stimulating repeatedly at the same locus, but significant differences occurred among responses obtained from identified parts of the basal ganglia. Stimulation in the putamen evoked tachypnoe, but no remarkable change in BP and HR. Stimulation in the caudate nucleus produced either tachypnoe or respiratory arrest accompanied by a slight change in BP and HR. Stimulation within the medial dorsal nucleus of the thalamus and the substantia nigra caused increase in BP, HR, and RR of different magnitude. The increase in BP failed to appear under the effect of alpha-adrenergic blockade. The effects of procaine, injected through the arterial cannula, did not interfere with the electrically elicited responses. All the cardiorespiratory responses to basal ganglia stimulation diminished or did not appear in deeply anaesthetised animals. We conclude that besides its involvement in motor processing, the basal ganglia circuitry exerts an influence on the central cardiorespiratory mechanisms.

Animals↗