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PubMed1998

Cholinesterases in cardiac ganglia and modulation of canine intrinsic cardiac neuronal activity.

Cholinergic neurotransmission plays a significant role in intrinsic cardiac ganglia with the action of acetylcholine being terminated by acetylcholinesterase (AChE, EC 3.1.1.7). Anatomical studies were performed to characterize neurons associated with AChE and a closely related enzyme, butyrylcholinesterase (BuChE, EC 3.1.1.8), in canine intrinsic cardiac ganglia. Histochemical staining for AChE and BuChE in canine right atrial neurons showed that there were four neuronal populations, namely, those that contained AChE only, BuChE only, both AChE and BuChE, and those that did not contain either enzymes. The neuronal activity of intrinsic cardiac neurons in response to substrates and inhibitors of cholinesterases were studied in anesthetized dogs. The activity of intrinsic cardiac neurons, as measured by changes in the number of action potentials, increased by local application of acetylcholine. However, local application of butyrylcholine led to a considerably greater increase in the activity of intrinsic cardiac neurons. In keeping with the neurochemical heterogeneity in intrinsic cardiac ganglia with respect to cholinesterases, the activity generated by most butyrylcholine-sensitive neurons was not influenced by acetylcholine and the activity generated by the most acetylcholine-sensitive neurons was not influenced by butyrylcholine. This suggests that these two agents preferentially influence different populations of intrinsic cardiac neurons. Enzyme kinetic studies demonstrated that canine AChE preferentially catalyzed the hydrolysis of acetylcholine while canine BuChE preferentially catalyzed the hydrolysis of butyrylcholine. Cholinesterase inhibitors Ro 2-1250 and Ro 2-0638 inhibited both canine cholinesterases, while huperzine A preferentially inhibited canine AChE and ethopropazine inhibited canine BuChE. The activity of neurons in the intrinsic cardiac ganglia significantly increased when Ro 2-1250 or Ro 2-0638 was administered locally. The activity of neurons was not affected when huperzine A or ethopropazine was administered, indicating that both cholinesterases must be inhibited to increase neuronal activity. In summary, these data show that in addition to AChE, intrinsic cardiac ganglia also contain distinct populations of neurons that are associated with BuChE, and the activity generated by these neurons is differentially influenced by their substrates. Because simultaneous inhibition of AChE and BuChE leads to increased neuronal activity, it is concluded that AChE- and BuChE-positive intrinsic cardiac neurons may act synergistically to influence the overall tonic activity of intrinsic cardiac ganglia.

Acetylcholine↗

PubMed1998

Bright basal ganglia in T1-weighted magnetic resonance images are frequent in patients with portal vein thrombosis without liver cirrhosis and not suggestive of hepatic encephalopathy.

BACKGROUND/AIMS: Deposition of paramagnetic substances in basal ganglia, resulting in increased signals in T1-weighted magnetic resonance images (bright basal ganglia), is frequently seen in liver cirrhosis. The present study describes the prevalence of bright basal ganglia and its clinical significance in patients with long-standing portal vein thrombosis in the absence of liver cirrhosis. METHODS: Six patients with angiographically proven complete portal vein thrombosis and cavernomatous transformation without signs of acute or chronic liver disease were studied by magnetic resonance imaging of the brain, neuropsychiatric evaluation, psychometric tests, electroencephalography, and determination of arterial ammonia levels and of serum manganese concentrations from peripheral venous blood. RESULTS: Five out of six patients demonstrated increased signal intensity in the basal ganglia. Overt portal-systemic encephalopathy was not noted prior to or at the time of evaluation. Normal EEG results were recorded in all patients. Only one of the six patients had pathological results in at least two out of four psychometric tests. This latter patient had had a large right-sided brain infarction. Arterial ammonia concentrations were normal in four of the six patients; one patient with increased ammonia levels had concomitant renal insufficiency with azotemia. The other four patients had no relevant concomitant diseases. Serum manganese levels were non-significantly increased compared with a control group (p=0.06), but they were significantly correlated to basal ganglia signal intensity (R=0.88; p=0.02). CONCLUSIONS: Our results demonstrate that bright basal ganglia primarily represent shunt-induced alterations. They are not directly associated with disturbed liver function nor with portal-systemic encephalopathy.

Adult↗

PubMed2002

Cysticercosis lesions in basal ganglia are common but clinically silent.

Movement disorders due to basal ganglia involvement by neurocysticercosis are rarely seen. To evaluate the frequency of basal ganglia location of cysticercotic cysts and its clinical manifestations, baseline MRI scans of 120 consecutive patients with active neurocysticercosis were reviewed and the presence and number of active cysticercosis lesions (viable cysts or enhancing lesions) in the basal ganglia were recorded and correlated with demographic and clinical data. Basal ganglia involvement was found in 32 cases (26.7%). The frequency of lesions in basal ganglia was related to the total number of lesions, ranging from 5% of patients with a single cysticerci, to 60% in patients with more than five parasites. Putamen and caudate nuclei were the most frequent sites of lesions. No significant difference between both hemispheres was observed. Basal ganglia localization is common in neurocysticercosis but it is rarely associated with clinical manifestations.

Adolescent↗

PubMed2003

Effect of endotoxin treatment on the expression of cyclooxygenase-2 and prostaglandin synthases in spinal cord, dorsal root ganglia, and skin of rats.

Peripheral inflammation causes upregulation of cyclooxygenase in the spinal cord and subsequent increase in prostaglandin biosynthesis. However, prostaglandin synthases, which are downstream of cyclooxygenase control the type of prostaglandin that is formed predominantly. Since there is little known about the regulation of prostaglandin synthases, the present study was conducted in order to determine the effect of endotoxin treatment on the expression of messenger RNA encoding interleukin 1beta, cyclooxygenase-2, and prostaglandin synthases mediating the formation of prostaglandin E(2) (membrane bound prostaglandin E synthase) and prostaglandin D(2) (lipocalin prostaglandin D synthase) in spinal cord, dorsal root ganglia and skin of rats. Endotoxin (2 mg/kg i.p.) induced the expression of interleukin-1beta, cyclooxygenase-2, and membrane bound prostaglandin E synthase messenger RNA in spinal cord, dorsal root ganglia, and skin as determined by reverse transcription polymerase chain reaction. In contrast, basal expression of lipocalin prostaglandin D synthase messenger RNA in spinal cord and dorsal root ganglia was not significantly altered by endotoxin. Dexamethasone (1 mg/kg s.c. at -18 h and -1 h) attenuated the effect endotoxin on the expression of interleukin-1beta, cyclooxygenase-2, and membrane bound prostaglandin E synthase messenger RNA in all tissues investigated, but did not significantly influence expression of lipocalin prostaglandin D synthase mRNA in spinal cord and dorsal root ganglia. In situ hybridisation histochemistry showed endotoxin-induced expression of cyclooxygenase-2 and membrane bound prostaglandin E synthase messenger RNA throughout gray and white matter of spinal cord sections. In dorsal root ganglia, expression of membrane bound prostaglandin E synthase seemed primarily located to non-neuronal cells, while cyclooxygenase-2 messenger RNA was not detectable. The results show that the immune response elicited by endotoxin induced cyclooxygenase-2 and membrane bound prostaglandin E synthase, but not lipocalin prostaglandin D synthase messenger RNA in spinal cord and dorsal root ganglia of rats. The distribution of cyclooxygenase-2 and membrane bound prostaglandin E synthase messenger RNA expressing cells suggests major involvement of non-neuronal cells in spinal prostaglandin biosynthesis. Determination of the regulation of enzymes downstream of cyclooxygenase at the messenger RNA level may represent a valuable tool to investigate effects of analgesic/anti-inflammatory drugs on the regulation of spinal prostaglandin biosynthesis.

Animals↗

PubMed2000

Pre- and postsynaptic localization of GABA(B) receptors in the basal ganglia in monkeys.

GABAergic neurotransmission involves ionotropic GABA(A) and metabotropic GABA(B) receptor subtypes. Although fast inhibitory transmission through GABA(A) receptors activation is commonly found in the basal ganglia, the functions as well as the cellular and subcellular localization of GABA(B) receptors are still poorly known. Polyclonal antibodies that specifically recognize the GABA(B)R1 receptor subunit were produced and used for immunocytochemical localization of these receptors at the light and electron microscope levels in the monkey basal ganglia. Western blot analysis of monkey brain homogenates revealed that these antibodies reacted specifically with two native proteins corresponding to the size of the two splice variants GABA(B)R1a and GABA(B)R1b. Preadsorption of the purified antiserum with synthetic peptides demonstrated that these antibodies recognize specifically GABA(B)R1 receptors with no cross-reactivity with GABA(B)R2 receptors. Overall, the distribution of GABA(B)R1 immunoreactivity throughout the monkey brain correlates with previous GABA(B) ligand binding studies and in situ hybridization data as well as with recent immunocytochemical studies in rodents. GABA(B)R1-immunoreactive cell bodies were found in all basal ganglia nuclei but the intensity of immunostaining varied among neuronal populations in each nucleus. In the striatum, interneurons were more strongly stained than medium-sized projection neurons while in the substantia nigra, dopaminergic neurons of the pars compacta were much more intensely labeled than GABAergic neurons of the pars reticulata. In the subthalamic nucleus, clear immunonegative neuronal perikarya were intermingled with numerous GABA(B)R1-immunoreactive cells. Moderate GABA(B)R1 immunoreactivity was observed in neuronal perikarya and dendritic processes throughout the external and internal pallidal segments. At the electron microscope level, GABA(B)R1 immunoreactivity was commonly found in neuronal cell bodies and dendrites in every basal ganglia nuclei. Many dendritic spines also displayed GABA(B)R1 immunoreactivity in the striatum. In addition to strong postsynaptic labeling, GABA(B)R1-immunoreactive preterminal axonal segments and axon terminals were frequently encountered throughout the basal ganglia components. The majority of labeled terminals displayed the ultrastructural features of glutamatergic boutons and formed asymmetric synapses. In the striatum, GABA(B)R1-containing boutons resembled terminals of cortical origin, while in the globus pallidus and substantia nigra, subthalamic-like terminals were labeled. Overall, these findings demonstrate that GABA(B) receptors are widely distributed and located to subserve both pre- and postsynaptic roles in controlling synaptic transmission in the primate basal ganglia.

Animals↗

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↗

PubMed1999

Thalamic interaction between the input and the output systems of the basal ganglia.

The striatal return through the thalamus is largely neglected in current studies dealing with basal ganglia function, and its role within this circuitry remains obscure. In this contribution the thalamus is regarded as an important place of interaction between the input and the output organization of the basal ganglia. In support of this idea, a brief overview is provided of some of the most recent findings concerning the thalamus in relation to the basal ganglia circuitry. In particular, we have focused on the thalamostriatal projections themselves, on the output of the basal ganglia to the thalamus and also on the overlapping territories between the thalamic projection of the output nuclei and the thalamostriatal neurons. These data support the existence of several thalamic feedback circuits within the basal ganglia neural system. Finally, some considerations are provided upon the functional significance of these thalamic feedback circuits in the overall organization of the basal ganglia.

Animals↗

PubMed2003

Syntactic language processing: ERP lesion data on the role of the basal ganglia.

The role of the basal ganglia in syntactic language processing was investigated with event-related brain potentials in fourteen neurologically impaired patients. Seven of these patients had basal ganglia lesions while 7 other patients primarily had lesions of the left temporo-parietal region excluding the basal ganglia. All patients listened to sentences that were either correct or included a verb argument structure violation. In previous experiments this type of violation elicited a biphasic pattern of an N400-P600 complex in young healthy participants. While the N400 may result from incorrect semantic-thematic role assignment, the P600 reflects the fact that verb information does not license the syntactic structure at present. Results of the patient experiment revealed a double dissociation: patients with left temporo-parietal lesions only show a P600, whereas patients with lesions of the basal ganglia showed no P600, but a negativity with extended duration that resembled an N400. The latter pattern not only confirms previous reports that the basal ganglia modulate the P600 but extends these results by showing that the N400 as a late semantic-thematic integration process appears partially modulated by the basal ganglia.

Adult↗

PubMed2001

Stereological study of the cells of dorsal root ganglia in male diabetic rats.

Most research on diabetes mellitus has focused on physiological and biochemical aspects of the peripheral nervous system, whilst little work has been done on morphological changes of the neurons. In the present study the effects of diabetes mellitus on cervical and lumbar dorsal root ganglia (C7 and L5) were investigated using modern stereological methods. Twelve adult male Sprague-Dawley rats were randomly divided into two groups. Each group contained six male rats. Diabetes was induced in the experimental group by intraperitoneal injection of 50 mg/kg streptozotocin. At the end of 6 weeks, the rats were fixed by whole body perfusion transcardially with a buffered formalin solution. The seventh cervical and fifth lumbar dorsal root ganglia were removed and immersed in buffered formalin. After tissue processing, the ganglia were embedded in cylindrical paraffin blocks. Isotropic uniform random sections were obtained using the orientator method. Sections (5 microm thick) were selected and stained with Heidenhain's azan. Volume of perikarya of A- and B-cells and their nuclei was estimated using the nucleator method. Before estimating the mean volume, the cells were sampled using the physical disector and point sampling method. Measurements showed that mean perikaryal and nuclear volume of A- and B-cells of dorsal root ganglia (C7 and L5) was reduced in diabetic rats (p<0.05). B-cell mean perikaryal volume in diabetic rats and A- and B-cell mean nuclear volume were reduced by 66% on average. The mean volume of A-cell perikarya was affected less than the others (average 33%). In addition, the difference between the perikaryal and nuclear volume of the seventh cervical and fifth lumbar dorsal root ganglia was not statistically significant. The present study, using stereological techniques, demonstrates reduced perikaryal and nuclear volume of the seventh cervical and fifth lumbar dorsal root ganglia in diabetic rats.

Animals↗

PubMed1984

Rapid accumulation of inositol phosphates in isolated rat superior cervical sympathetic ganglia exposed to V1-vasopressin and muscarinic cholinergic stimuli.

An accumulation of 3H-labelled inositol phosphates is observed when prelabelled rat superior cervical sympathetic ganglia are exposed to [8-arginine]vasopressin or to muscarinic cholinergic stimuli. The response to vasopressin is much greater than the response to cholinergic stimuli. The response to vasopressin is blocked by a V1-vasopressin antagonist, and oxytocin is a much less potent agonist than vasopressin. Vasopressin causes no increase in the cyclic AMP content of ganglia. These ganglia therefore appear to have functional V1-vasopressin receptors that are capable of activating inositol lipid breakdown, but no V2-receptors coupled to adenylate cyclase. The first [3H]inositol-labelled products to accumulate in stimulated ganglia are inositol trisphosphate and inositol bisphosphate, suggesting that the initiating reaction in stimulated inositol lipid metabolism is a phosphodiesterase-catalysed hydrolysis of phosphatidylinositol 4,5-bisphosphate (and possibly also phosphatidylinositol 4-phosphate). This response to exogenous vasopressin occurs in ganglia incubated in media of reduced Ca2+ concentration. The physiological functions of the V1-vasopressin receptors of these ganglia remain unknown.

Animals↗

PubMed2002

Insulin-like growth factor-II/Mannose-6-phosphate receptor in the spinal cord and dorsal root ganglia of the adult rat.

The insulin-like growth factor-II/mannose-6-phosphate (IGF-II/M6P) receptor is a multifunctional transmembrane glycoprotein, which interacts with a number of molecules, including IGF-II and M6P-containing lysosomal enzymes. The receptor is widely distributed throughout the brain and is known to be involved in lysosomal enzyme trafficking, cell growth, internalization and degradation of IGF-II. In the present study, using autoradiographic, Western blotting and immunocytochemical methods, we provide the first report that IGF-II/M6P receptors are discretely distributed at all major segmental levels of the spinal cord and dorsal root ganglia of the adult rat. In the spinal cord, a high density of [(125)I]IGF-II binding sites was evident in the ventral horn (lamina IX) and in areas around the central canal (lamina X), whereas intermediate grey matter and dorsal horn were associated with moderate receptor levels. The dorsal root ganglia exhibited rather high density of [(125)I]IGF-II binding sites. Interestingly, meninges present around the spinal cord displayed highest density of [(125)I]IGF-II binding compared to any given region of the spinal grey matter or the dorsal root ganglia. Western blot results indicated the presence of the IGF-II/M6P receptor at all major levels of spinal cord and dorsal root ganglia, with little segmental variation. At the cellular level, spinal motorneurons demonstrated the most intense IGF-II/M6P receptor immunoreactivity, followed by interneurons in the intermediate region and deeper dorsal horn. Some scattered IGF-II/M6P immunoreactive fibers were found in the superficial laminae of the dorsal horn and dorsolateral funiculus. The meninges of the spinal cord also seemed to express IGF-II receptor immunoreactivity. In the dorsal root ganglia, receptor immunoreactivity was evident primarily in a subset of neurons of all diameters. These results, taken together, provide anatomical evidence of a role for the IGF-II/M6P receptor in general cellular functions such as transport of lysosomal enzymes and/or internalization followed by clearance of IGF-II in the spinal cord and dorsal root ganglia.

Animals↗

PubMed1997

Perivascular spaces in the basal ganglia of the human brain: their relationship to lacunes.

There is evidence for lymphatic drainage of interstitial fluid from the brain along perivascular spaces in a number of mammalian species. Ultrastructural studies suggest that there are similar drainage pathways in the human cerebral cortex. Perivascular spaces in the basal ganglia, however, differ from those in the cortex in that they dilate to form lacunes and rarely accumulate beta-amyloid (amyloid angiopathy) in Alzheimer's disease; in the cortex, lacunes are rare but amyloid angiopathy is common. The aim of the present study is to compare the structure of perivascular spaces in the basal ganglia and at the anterior perforated substance with perivascular spaces in the cerebral cortex. Eight postmortem brains from patients aged 23-80 years (mean 68 y) were examined by light microscopy, by scanning and transmission electron microscopy and by direct visualisation of etched paraffin blocks. The results show that arteries in the basal ganglia are surrounded by 2 distinct coats of leptomeninges separated by a perivascular space which is continuous with the perivascular space around arteries in the subarachnoid space. The inner layer of leptomeninges closely invests the adventitia of the vessel wall and the outer layer is continuous with the pia mater on the surface of the brain at the anterior perforated substance. Veins in the basal ganglia have no outer layer of leptomeninges and thus the perivascular space is continuous with the subpial space. The anatomy of the periarterial spaces in the basal ganglia differs significantly from that in the cerebral cortex where there is only a single periarterial layer of leptomeninges. Differences in structure of perivascular spaces around arteries may reflect relative efficiencies in the drainage of interstitial fluid from different sites in the brain. Furthermore, the structure of the perivascular spaces may contribute to the relatively high frequency of lacunes in the basal ganglia, and the low frequency of amyloid angiopathy at this site in Alzheimer's disease.

Adult↗

PubMed2001

Prevalence of herpesviruses in cranial nerve ganglia.

A number of cranial nerve disorders are known to result from viral infection or reactivation, including Bell's palsy, Ramsay Hunt syndrome and herpetic laryngitis. The consequences of these diseases are well established although the patient population at risk is not. Prevalence studies in the general population are an initial step toward defining individuals at risk. The aim of this study was to determine the prevalence of herpesvirus DNA in cranial nerve ganglia in a random population sample. Qualitative molecular biologic analysis using polymerase chain reaction assay of the trigeminal, geniculate, vestibular, spiral and vagal ganglia was used in 18 randomly selected fresh cadaver heads. Herpes simplex virus (HSV) DNA was detected in 42% of all ganglia surveyed. Varicella zoster virus (VZV) DNA was detected in 44% of all ganglia. The difference in the prevalence rate between viruses was not significant (p = 0.63). At least 1 of the 2 viruses was found in 65% of all ganglia. Both HSV and VZV can commonly be recovered from cranial nerve ganglia. In order to confirm a viral etiology for various cranial nerve disorders, demonstration of a significant difference in prevalence of the viruses in specimens from afflicted individuals will be necessary.

Adolescent↗

PubMed2006

Basal ganglia lesions following carbon monoxide poisoning.

PRIMARY OBJECTIVES: Carbon monoxide (CO) is the most common cause of poisoning and may result in basal ganglia lesions. This study reviewed the literature of carbon monoxide poisoning and basal ganglia lesions and prospectively assessed the prevalence of basal ganglia lesions in a cohort of patients with CO poisoning. RESEARCH DESIGN: Literature review and prospective cohort study. METHODS: This study conducted a comprehensive review of the literature and assessed 73 CO-poisoned patients for basal ganglia lesions on sequential MR scans. Magnetic resonance scans were obtained on day 1, 2 weeks and 6 months post-CO poisoning. RESULTS: The literature review found basal ganglia lesions occur in 4-88% of subjects. Only one patient was found with globus pallidus lesions at 2 weeks and 6 months following CO poisoning, that were not present on the initial day 1 MR scan. CONCLUSIONS: Basal ganglia lesions, including lesions of the globus pallidus, may be less common than previously reported.

Adolescent↗

PubMed2006

Observation of the fast response of a magnetic resonance signal to neuronal activity: a snail ganglia study.

We observed the response of a magnetic resonance signal to neuronal activity in dissected snail ganglia to investigate faster responding components than the blood oxygenation level dependent (BOLD) component. To eliminate the BOLD component completely from the magnetic resonance signal, we used dissected snail ganglia which have non-magnetic hemocyanin, other than hemoglobin, as an oxygen carrying protein. To activate the snail ganglia in synchronization with the magnetic resonance signal measurement, we applied 30 Hz electrical stimulation with a pulse width of 2 s to the ganglia just before the 90 degrees RF pulse. The increase of neuronal activity in the snail ganglia after the electrical stimulation was confirmed with extracellular potential recording. The magnetic resonance signal intensity, measured with the volume selection pulse sequence in a 3.0 T MRI, decreased by about 2.97 +/- 1.10% when the ganglia were activated by the electrical stimulation. We think that the MRI signal decrease is partly due to the magnetic field produced by the neuronal current and partly due to the Lorentz force exerted on the neurons when they were firing.

Animals↗

PubMed1996

The basal ganglia and apraxia.

Ever since Liepmann's original descriptions at the beginning of the century apraxia has usually been attributed to damage confined to the cerebral cortex and/or cortico-cortical connecting pathways. However, there have been suggestions that apraxia can be due to deep subcortical lesions, which raises the question as to whether damage to the basal ganglia or thalamus can cause apraxia. We therefore analysed 82 cases of such 'deep' apraxias reported in the literature. These reports consisted of a small number (n=9) of cases studied neuropathologically, and a much larger group (n=73) in which CT or MRI was used to identify the size and extent of the lesion. The reports were subdivided into (i) those with small isolated lesions which involved nuclei of the basal ganglia or thalamus only, and not extending to involve periventricular or peristriatal white matter; (ii) those with large lesions which involved two or more of the nuclei, or one or more of these deep structures plus damage to closely adjacent areas including the internal capsule, periventricular or peristriatal white matter; and (iii) lesions sparing basal ganglia and thalamus but involving adjacent white matter. The main conclusions to be drawn from this meta-analysis are that lesions confined to the basal ganglia (putamen, caudate nucleus and globus pallidus) rarely, if ever, cause apraxia. Lesions affecting the lenticular nucleus or putamen nearly always intruded into the adjacent lateral white matter to involve association fibres, in particular those of the superior longitudinal fasciculus and frontostriatal connections. Apraxia occurred with deep lesions of the basal ganglia apparently sparing white matter in only eight out of the 82 cases. Apraxia was most commonly seen when there were lesions in the lenticular nucleus or putamen (58 out of 72 cases) with additional involvement of capsular, and particularly of periventricular or peristriatal, white matter. Lesions of the globus pallidus (no cases) or caudate nucleus (three cases) rarely caused apraxia. The caudate lesions also had white matter involvement. Indeed, involvement of periventricular white matter alone caused apraxia. The vast majority of cases described with apraxia associated with deep lesions were in the left, dominant hemisphere. Ideomotor apraxia was described in most reports (72 out of 82 cases). Orofacial apraxia was less common (37 cases), usually with ideomotor apraxia. Ideational apraxia was rare (five cases), all with ideomotor apraxia. Apraxia was either bilateral or involved the left hand if there was a right hemiparesis, in those cases where descriptions were available. Lesions of the thalamus can sometimes cause apraxia (26 cases), even if there is no apparent involvement of white matter (12 cases). Small lesions confined to the thalamus can also sometimes cause apraxia (eight cases). The role of the thalamus in higher order motor control and apraxia remains to be determined. It is suggested that the term limb-kinetic apraxia should be retained to describe motor deficits in planning 'what to do', 'how to do it' and 'when to do it'; decisions which appear to involve activation of a complex distributed network of dorsolateral prefrontal cortex, supplementary motor areas, anterior cingulate regions and lateral premotor cortex. Such deficits need to be quantified. If they are present in patients with basal ganglia disease, over and above classical akinesia, bradykinesia and hypokinesia, then such patients could be said to exhibit limb-kinetic apraxia.

Apraxias↗

PubMed2003

Dysfunction of the basal ganglia, but not the cerebellum, impairs kinaesthesia.

Precise knowledge about limb position and orientation is essential for the ability of the nervous system to plan and control voluntary movement. While it is well established that proprioceptive signals from peripheral receptors are necessary for sensing limb position and motion, it is less clear which supraspinal structures mediate the signals that ultimately lead to the conscious awareness of limb position (kinaesthesia). Recent functional imaging studies have revealed that the cerebellum, but not the basal ganglia, are involved in sensory processing of proprioceptive information induced by passive and active movements. Yet psychophysical studies have suggested a prominent role of the basal ganglia in kinaesthesia. This study addresses this apparent dichotomy by investigating the contributions of the cerebellum and the basal ganglia to the perception of limb position. Using a passive movement task, we examined the elbow position sense in patients with a dysfunction of the basal ganglia (Parkinson's disease, n = 9), patients with cerebellar degeneration [spinocerebellar ataxia (SCA) types 6 and 8, n = 6] and age-matched healthy control subjects (n = 11). In comparison with healthy control subjects, Parkinson's disease patients, but not SCA patients, were significantly impaired in the ability to detect displacements correctly. A 1 degrees forearm displacement was correctly recognized in >75% of trials by control subjects and SCA patients, but only in 55% of Parkinson's disease patients. Only at 6 degrees displacement did Parkinson's disease patients exhibit a response rate similar to those of the two other groups. Thresholds for 75% correct responses were 1.03 degrees for controls, 1.15 degrees for cerebellar patients and 2.10 degrees for Parkinson's disease patients. This kinaesthetic impairment significantly correlated with the severity of disease in Parkinson's disease patients, as determined by the Unified Parkinson's Disease Rating Scale (r = -0.7, P = 0.03) and duration of disease (r = -0.7, P = 0.05). In contrast, there was no significant correlation between performance and the daily levodopa equivalent dose. These results imply that an intact cerebro-basal ganglia loop is essential for awareness of limb position and suggest a selective role of the basal ganglia but not the cerebellum in kinaesthesia.

Adult↗

PubMed2006

The basal ganglia are hyperactive during the discrimination of tactile stimuli in writer's cramp.

Writer's cramp is a focal hand dystonia that specifically affects handwriting. Though writer's cramp has been attributed to a dysfunction of the basal ganglia, the role of the basal ganglia in the pathogenesis of writer's cramp remains to be determined. Seventeen patients with writer's cramp (nine females; age range: 24-71 years) and 17 healthy individuals (six females; age range: 27-68 years) underwent functional MRI (fMRI) while they discriminated the orientation of gratings delivered to the tip of the right index finger. Statistical parametric mapping was used to analyse the fMRI data. The significance level was set at a corrected P-value of 0.05. Relative to healthy controls, patients with writer's cramp showed a widespread bilateral increase in task-related activity in the putamen, caudate nucleus, internal globus pallidus and lateral thalamus. In these areas, hyperactivity was more pronounced in patients who had recently developed writer's cramp. The enhanced response of the basal ganglia to tactile input from the affected hand is compatible with the concept of impaired centre-surround inhibition within the basal ganglia-thalamic circuit and may lead to an excessive activation of sensorimotor cortical areas during skilled movements affected by dystonia. Outside the basal ganglia, dystonic patients showed task-related overactivity in visual cortical areas, left anterior insula and right intraparietal sulcus, but not in the primary or secondary sensory cortex. In addition, task-related activity in the cerebellar nuclei, posterior vermis, right paramedian cerebellar hemisphere and dorsal pons was inversely related with the severity of hand dystonia. Regional activity in these areas may reflect secondary adaptive reorganization at the systems level to compensate for the dysfunction in the basal ganglia-thalamic loop.

Adult↗