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Signal Attenuation as a Rat Model of Obsessive Compulsive Disorder
Published on: January 9, 2015
Secondary obsessive-compulsive disorder related to diaschisis after pontine infarction, successfully treated with
Tokuzo Matsui1, Sanjaya Saxena, Joji Kawabe
1Department of Neuropsychiatry, Graduate School of Medicine, Osaka City University, Osaka, Japan. qzg03064@nifty.ne.jp
Abstract:
This report describes a case of secondary obsessive-compulsive disorder related to diaschisis after pontine infarction. A 71-year-old male developed obsessive images, after a pontine infarction. A brain magnetic resonance imaging scan showed a low intensity area in the right pons on T1-weighted image, while brain single photon emission computed tomography showed low cerebral blood flow in the temporal lobe as well as the pons. In this case, infarction in the pons appeared to cause dysfunction in the temporal lobe via the neural projection network, an example of so-called 'diaschisis'. This case suggests that brainstem infarction and decreased temporal lobe perfusion can lead to secondary obsessive-compulsive disorder.
Insights
Pontine infarction can lead to secondary obsessive-compulsive disorder (OCD) through diaschisis, a neurological condition affecting distant brain areas. This case highlights the link between brainstem lesions and temporal lobe dysfunction causing OCD symptoms.
Area of Science:
- Neurology
- Neuroscience
- Psychiatry
Background:
- Obsessive-compulsive disorder (OCD) is a mental health condition characterized by obsessions and compulsions.
- Secondary OCD can arise from various neurological conditions.
- Pontine infarction, a stroke affecting the pons in the brainstem, is a less common cause.
Observation:
- A 71-year-old male presented with new-onset obsessive images following a pontine infarction.
- Brain imaging revealed a lesion in the right pons (T1-weighted MRI) and reduced cerebral blood flow in the temporal lobe and pons (SPECT).
Findings:
- The pontine infarction likely caused diaschisis, affecting the temporal lobe via neural pathways.
- This temporal lobe dysfunction, secondary to the brainstem lesion, is hypothesized to have triggered OCD symptoms.
Implications:
- This case suggests a potential mechanism linking brainstem infarction and secondary OCD.
- It underscores the importance of considering cerebrovascular events in the differential diagnosis of secondary OCD.
- Further research into diaschisis following brainstem strokes may elucidate other associated neuropsychiatric disorders.
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