Atrophy in Thalamus Linked to More Severe Non-motor Problems in Parkinson’s Patients

brain regions

People with severe non-motor symptoms related to Parkinson’s disease (PD) have a smaller thalamus compared to those with similar but mild to moderate symptoms, a brain imaging study suggests.

Sleeping and gastrointestinal problems are also tied to atrophy (shrinking) of the thalamus, a part of the inner brain known to process motor signals and to regulate consciousness, alertness, and sleep.

The study, “Sleep disturbances and gastrointestinal dysfunction are associated with thalamic atrophy in Parkinson’s disease,” was published in the journal BMC Neuroscience

Parkinson’s is marked by a progressive loss of coordination and movement. In addition to difficulties in movement (motor symptoms), it can cause a variety of non-motor symptoms such as sleep problems, depression, gastrointestinal and urinary problems, and difficulty thinking (cognitive impairment).

Techniques such as magnetic resonance imaging (MRI) help to diagnose PD through brain scans, and they can also help identify structural changes in the brain — like changes in thickness or volume — associated with its non-motor symptoms.

But the exact location of specific brain areas linked to non-motor symptoms is still unclear. 

Researchers recruited 41 patients diagnosed with idiopathic (unknown origin) PD at the Movement Disorders clinics at King’s College Hospital in London. All were analyzed through MRI brain scans.

None of these patients chosen showed signs of mild PD cognitive impairments or disease-related dementia, and they had no history of neurological or psychiatric disorders.

Patients were first assessed by medical staff using the Non-motor Symptoms Scale for PD (NMSS), then self-assessed using the Non-motor Symptoms Questionnaire (NMSQ). The Beck Depression Inventory-II (BDI-II) and the Hamilton Depression Rating Scale (HDRS) evaluated neuropsychiatric symptoms.

Motor symptoms stages were determined with the Hoehn & Yahr (H&Y) scale, general cognitive status was assessed using the Mini Mental Status Examination (MMSE), and quality of life (QoL) was measured by patients completing the 39-item PD Questionnaire (PDQ-39).

All were required to stop taking dopamine-related medications the night before the scans to avoid involuntary movements caused by side effects. 

Patients were then divided into two groups based on their NMSS scores. A total of 23 patients who scored 40 or below were considered to have mild to moderate non-motor Parkinson’s symptoms, while 18 who scored 41 or above were defined as severe. 

Results showed that, compared to those with mild to moderate symptoms, those with severe non-motor symptoms were older, had the disease longer, were using higher doses of medication, had higher H&Y scores, and reported a lower QoL. Severe non-motor PD patients also scored more poorly in the sleep and fatigue sections of the NMSS. 

MRI scans were taken, and the cortical (outer brain) thickness and subcortical (inner brain) volumes were calculated and compared with patient assessments.

Analyses revealed that the inner brain’s thalamus was significantly smaller in volume (thalamic atrophy) in PD patients with severe non-motor symptoms, compared to those with mild to moderate symptoms. 

Other areas of the inner brain, including the hippocampus, the amygdala, were similar between the two groups. No differences in the thickness of the outer brain were seen. 

Researchers then divided patients into two groups based on sleep/fatigue problems and gastrointestinal tract dysfunction. Compared to those without these problems, a smaller thalamus was significantly associated with sleep and gastrointestinal disturbances. 

“This is the first study showing an association between higher non-motor symptom burden and thalamic atrophy in PD. Among the non-motor symptoms, sleep/fatigue disturbances and gastrointestinal dysfunction were the non-motor symptoms that drove this correlation,” the researchers wrote.

The team, however, noted that further studies with larger numbers of PD patients are needed to confirm these findings, and use specific scales to measure nighttime and daytime sleep problems and tools that capture gastrointestinal dysfunction.

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Psychosis in Parkinson’s Linked to Volume Changes in Specific Area of Brain, Study Says

psychosis in Parkinson's

Psychosis and cognitive impairment in patients with Parkinson’s disease may be linked to structural changes in the brain, namely a decrease in volume of an area that controls memory formation, a study suggests.

The study, “Hippocampal subfield atrophy in patients with Parkinson’s disease and psychosis,” was published in the Journal of Neural Transmission.

Psychosis, which usually manifests as visual hallucinations, is one of the most frequently observed non-motor symptoms of Parkinson’s disease.

More than 50 percent of Parkinson’s patients will experience psychosis in their lifetimes, and the condition is associated with poor quality of life and more use of healthcare resources.

The causes underlying psychosis in Parkinson’s disease remain unclear, but some studies suggest it may be linked to structural and functional alterations of the hippocampus, a brain region that plays a key role in memory formation.

Using magnetic resonance imaging (MRI), researchers analyzed the hippocampus of 51 Parkinson’s patients without psychosis, 42 Parkinson’s patients with psychosis, and 48 healthy people matched by age, gender, and education, used as controls.

Patients were recruited from the National Institute of Mental Health and Neurosciences in Bangalore, India.

Additional parameters analyzed included participants’ overall cognitive performance, measured using the Montreal Cognitive Assessment Scale (MoCA), and frontal executive functions — the skills a person uses to plan, organize and complete tasks — evaluated using the frontal assessment battery (FAB), which assesses the brain’s frontal lobe function.

Overall cognitive performance was significantly higher in healthy controls than in Parkinson’s patients both with and without psychosis. There were no significant differences in cognition between the Parkinson’s patients, regardless of whether they had psychosis or not.

FAB scores were also significantly lower in both groups of Parkinson’s patients than controls, highlighting an impairment in executive functions in patients both with and without psychosis.

Researchers observed that the overall volume of the hippocampus was reduced in Parkinson’s patients with psychosis compared with healthy controls, and that the volumes of different subzones in the hippocampus of these patients correlated with psychosis severity and cognitive functions.

However, Parkinson’s patients with psychosis had increased volume of a specific region within the hippocampus called the hippocampal fissure. The higher the volume in this area, the lower the capacity of visual memory and visuospatial functions.

Mouse studies have previously demonstrated that an increase in hippocampal fissure volume is highly correlated with a decrease in overall hippocampal volume, and can be considered a radiological hallmark of ongoing brain atrophy.

“We demonstrated that the trajectory of psychosis severity could be mapped using hippocampal subfield volumes,” the researchers wrote.

These results support the involvement of specific hippocampal regions in psychosis and cognitive impairment in Parkinson’s disease.

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Source: Parkinson's News Today