Neuropsychiatric disorders, myoclonus, and dystonia in calcification of basal ganglia pathways

Lauterbach, Edward C.; Spears, T.Elisabeth; Prewett, Michael J.; Price, Spencer T.; Jackson, J.G.; Kirsh, Alan D.

doi:10.1016/0006-3223(94)90038-8

Cited by 35 publications

(20 citation statements)

References 43 publications

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“…Finally, basal ganglia lesions from a variety of causes can result in the development of psychiatric symptoms. Lesions of the caudate have been associated with behavioral changes (Mendez et al 1989;Narumoto et al 2005) and those of the globus pallidus have been associated with cognitive dysfunction (Lauterbach et al 1994) as well as auditory hallucinations, anxiety and paranoia (Lauterbach et al 1994). The development of affective symptoms have been reported after basal ganglia stroke (Turecki et al 1993;Berthier et al 1996), degenerative changes of thalamus and putamen (Parashos et al 1993), as well as lesions of the caudate, (Starkstein et al 1990;Bhatia et al 1993;Gluck-Vanlaer et al 1996), globus pallidus (Bhatia et al 1993;Martinelli et al 1993;Lauterbach et al 1994Lauterbach et al , 1997a and substantia nigra (Bhatia et al 1993).…”

Section: Emotional Controlmentioning

confidence: 98%

Cortico-basal ganglia circuitry: a review of key research and implications for functional connectivity studies of mood and anxiety disorders

Marchand

2010

Brain Struct Funct

116

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There is considerable evidence that dysfunction of the cortico-basal ganglia circuits may be associated with several mood and anxiety disorders. However, it is unclear whether circuit abnormalities contribute directly either to the neurobiology of these conditions or to the manifestation of symptoms. Understanding the role of these pathways in psychiatric illness has been limited by an incomplete characterization of normal function. In recent years, studies using animal models and human functional imaging have greatly expanded the literature describing normal cortico-basal ganglia circuit function. In this paper, recent key studies of circuit function using human and animal models are reviewed and integrated with findings from other studies conducted over the previous decades. The literature suggests several hypotheses of cortico-basal ganglia circuitry function in mood and anxiety disorders that warrant further exploration. Hypotheses are proposed herein based upon the cortico-basal ganglia mechanisms of: (1) feedforward and feedback control, (2) circuit integration and (3) emotional control. These are presented as models of circuit function, which may be particularly relevant to future investigations using neuroimaging and functional connectivity analyses.

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Section: Emotional Controlmentioning

confidence: 98%

Cortico-basal ganglia circuitry: a review of key research and implications for functional connectivity studies of mood and anxiety disorders

Marchand

2010

Brain Struct Funct

116

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“…Also, spasticity, gait disorder, speech impairment, dementia, parkinsonism, chorea, tremors, dystonia, myoclonus and coma are present. Papilledema of intracranial hypertension, Pleocytosis of CSF, paroxysmal Choreothetosis and paroxysmal dystonic Choreoathetosis have also been reported [50]. …”

Section: All Etiological Factors Were Combined In Tablementioning

confidence: 99%

Fahr’s syndrome: literature review of current evidence

Saleem

Aslam

Anwar

et al. 2013

Orphanet J Rare Dis

198

210

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Fahr’s disease or Fahr’s syndrome is a rare, neurological disorder characterized by abnormal calcified deposits in basal ganglia and cerebral cortex. Calcified deposits are made up of calcium carbonate and calcium phosphate, and are commonly located in the Basal Ganglia, Thalamus, Hippocampus, Cerebral cortex, Cerebellar Subcortical white matter and Dentate Nucleus. Molecular genetics of this disease haven’t been studied extensively; hence evidence at the molecular and genetic level is limited. Fahr’s disease commonly affects young to middle aged adults. Etiology of this syndrome does not identify a specific agent but associations with a number of conditions have been noted; most common of which are endocrine disorders, mitochondrial myopathies, dermatological abnormalities and infectious diseases. Clinical manifestations of this disease incorporate a wide variety of symptoms, ranging from neurological symptoms of extrapyramidal system to neuropsychiatric abnormalities of memory and concentration to movement disorders including Parkinsonism, chorea and tremors amongst others. Diagnostic criteria for this disease has been formulated after modifications from previous evidence and can be stated briefly, it consist of bilateral calcification of basal ganglia, progressive neurologic dysfunction, absence of biochemical abnormalities, absence of an infectious, traumatic or toxic cause and a significant family history. Imaging modalities for the diagnosis include CT, MRI, and plain radiography of skull. Other investigations include blood and urine testing for hematologic and biochemical indices. Disease is as yet incurable but management and treatment strategies mainly focus on symptomatic relief and eradication of causative factors; however certain evidence is present to suggest that early diagnosis and treatment can reverse the calcification process leading to complete recovery of mental functions. Families with a known history of Fahr’s disease should be counseled prior to conception so that the birth of affected babies can be prevented. This review was written with the aim to remark on the current substantial evidence surrounding this disease.

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“…More recently, task-based fMRI studies have associated atypical striatal activation to anxiety (PerezEdgar et al, 2013). Additionally, the globus pallidus has been linked to anxiety disorders based on lesion studies (Lauterbach et al, 1994) and emotional processing (Lorberbaum et al, 2004) based on reports from Positron Emission Tomography (PET). Furthermore, PET studies have reported cerebral blood flow (CBF) changes, specific to the striatum, during anticipatory anxiety to electrical shock (Hasler et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Hyper-Connectivity of Subcortical Resting-State Networks in Social Anxiety Disorder

et al. 2014

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Neuropsychiatric disorders, myoclonus, and dystonia in calcification of basal ganglia pathways

Cited by 35 publications

References 43 publications

Cortico-basal ganglia circuitry: a review of key research and implications for functional connectivity studies of mood and anxiety disorders

Cortico-basal ganglia circuitry: a review of key research and implications for functional connectivity studies of mood and anxiety disorders

Fahr’s syndrome: literature review of current evidence

Hyper-Connectivity of Subcortical Resting-State Networks in Social Anxiety Disorder

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