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Published on: December 24, 2013
Obsessive-compulsive disorder in Huntington's disease
1Department of Neurology, UCLA School of Medicine.
Insights
Obsessive-compulsive disorder (OCD) can manifest in patients with Huntington's disease (HD). Neurological disorders affecting the frontal lobe, caudate nucleus, and globus pallidus circuits may mediate OCD symptoms.
Area of Science:
- Neuroscience
- Neurology
- Psychiatry
Background:
- Huntington's disease (HD) is a progressive neurodegenerative disorder.
- Obsessive-compulsive disorder (OCD) is characterized by intrusive thoughts and repetitive behaviors.
- The neurological underpinnings of OCD in conjunction with other neurological conditions are not fully understood.
Observation:
- Two cases of Huntington's disease (HD) patients presenting with disabling obsessive-compulsive disorder (OCD) are described.
- The OCD symptoms were characterized by repetitive, stereotyped, complex, and egodystonic behaviors.
- A review of other neurological syndromes associated with OCD, including Gilles de la Tourette syndrome and various brain injuries, was conducted.
Findings:
- The study suggests that the frontal lobe, caudate nucleus, and globus pallidus form a critical circuit involved in mediating OCD symptoms.
- Shared features among neurological disorders manifesting OCD include excitatory subcortical output to the cortex.
- This highlights a potential common pathway for OCD symptomatology across diverse neurological conditions.
Implications:
- Understanding the neurocircuitry of OCD in HD may lead to targeted therapeutic interventions.
- Identifying shared neurological mechanisms can advance the treatment of OCD in various neurological disorders.
- Further research into the cortico-striatal-pallidal pathways is warranted for both HD and OCD treatment strategies.
Abstract:
Two patients with Huntington's disease (HD) and obsessive-compulsive disorder (OCD) are reported. The OCD was manifested by repetitive, stereotyped, complex, egodystonic behaviors that were disabling. These cases and other neurological syndromes with OCD (Gilles de la Tourette syndrome, neuroacanthocytosis, postencephalitic parkinsonism, caudate infarction, carbon monoxide poisoning, manganese intoxication, anoxia, progressive supranuclear palsy, Sydenham's chorea, and frontal lobe lesions) indicate that the frontal lobe, caudate nucleus, and globus pallidus are members of a complex circuit that plays a key role in mediating the symptoms of OCD. Evidence of excitatory subcortical output to cortex is shared by many neurological disorders manifesting OCD.
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