Clinical History: Deterioration of gait with freezing episodes and tremor in legs. Difficulty initiating movement. Leg rigidity worse on the left side.
NM Brain DAT scan 123I-ioflupane SPECT
15/06/2023, 11:45
The DaTSCAN demonstrates balance striatal loss to the caudate and putamina nuclei in the striata with relative increase in background tracer uptake.
This appearance is consistent with a loss of the pre-synaptic dopaminergic terminals.
This results in balance loss of tracer uptake demonstrating a ‘weak comma’ shaped appearance with high levels of background activity.
This appearance is abnormal and would be supportive of a diagnosis of idiopathic Parkinson’s disease or a Parkinsonian syndrome.
Dr Emma Owens
Consultant Radiologist
East Sussex Healthcare NHS Trust
MRI Head
17/06/2023, 16:20
Final Report
CLINICAL INFORMATION
Six year history of gait impairment. Wide-based gait. Difficulty initiating movement. Leg rigidity.
FINDINGS
Standard sequences of the brain. No previous for comparison.
There are couple of tiny nonspecific subcortical white matter abnormalities which are within normal limits for age. There is no mass lesion or infarction. There is no acute intracranial abnormality. The vascular flow voids appear normal. Normal appearances of the ventricles and extra-axial CSF spaces. The pituitary gland, corpus callosum and craniocervical junction appear normal. There is no selective brainstem atrophy. The basal ganglia appear unremarkable in volume. There is no abnormal mineralisation.
There is no diffusion abnormality.
CONCLUSION
There is no significant intracranial abnormality.
Dr Robert McCreary
Consultant Neuroradiologist
MRI Spine whole
17/06/2023, 16:20
Final Report
CLINICAL INFORMATION
Six year history of gait instability.
FINDINGS
Standard sequences of the whole spine. No previous for comparison.
Cervical spine. There are some spondylotic changes throughout the cervical spine with disc and facet joint degenerative change. There is no cord compression or signal change. There is multilevel neural foraminal stenosis particularly on the left with likely compression of the exiting left C 4, C5 and possibly also the left C6 exiting nerve root. No convincing compression on the right. The spinal cord returns normal signal. Normal cervicomedullary junction and visualised posterior fossa structures. Normal appearances of the soft tissues of the neck.
The thoracic spine is normally aligned with normal marrow signal throughout. There are no significant degenerative changes and there is no evidence of neural compression. The thoracic cord is normal.
The lumbar spine is normally aligned with normal marrow signal throughout. There are very minimal degenerative changes particularly affecting the facet joints however there is no evidence of neural compression.
The cauda equina nerve roots are normal. The conus terminates at the L1 level. There is no paraspinal mass lesion or collection. There is diverticulosis of the sigmoid colon.
CONCLUSION
Minor degenerative changes particularly affecting the facet joints within the cervical and lumbar spine. There is no cord compression or signal change. There is foraminal stenosis on the left affecting several levels as described above.
Dr Robert McCreary
Consultant Neuroradiologist
Good afternoon everyone … I thought I would go through how I got my first Parkinson’s diagnosis & what it was & how a Parkinson’s diagnosis was arrived at in my case & how my second Parkinson’s diagnosis was done last Thursday 8th May 2025. The neurologist I saw on Thursday had not seen the three scans I had done in June 2023.
Having examined them he may come to a different conclusion.
The three scan reports I had done in June 2023 are above at the top of the page. Fairly self explanatory I think & logical that they came to the “This appearance is abnormal and would be supportive of a diagnosis of idiopathic Parkinson’s disease or a Parkinsonian syndrome.”
My first Parkinson’s diagnosis was a bit of a blur. The neurologist was an NHS locum from Armenia, he wore a face mask, I am a bit deaf & English is not his first language & he is not a Parkinson’s specialist.
My second neurologist on Thursday was excellent. The diagnosis examination actually starts when he comes into the waiting room. He looks at how I get up from my chair, my posture & how I walk to his examining room. He asked me all the usual questions on my history & how things have been lately & what is troubling me.
Then comes the physical exam … My balance, my dexterity, my eyes, the feelings in my feet, my eyes, my reflexes etc …
He saw me double lace up my shoes & said I did it incredibly quickly & easily.
Conclusion … I’ve not been given it officially yet as he hasn’t seen the three mri scans but he thinks I have Vascular Parkinson’s. He says all my Parkinson’s symptoms are in the bottom half of my body.
Atypical Parkinson’s and vascular Parkinson’s, both forms of Parkinsonism, are distinct conditions characterized by Parkinsonian symptoms, but they differ in their causes and progression. Atypical Parkinson’s encompasses various disorders like Multiple System Atrophy (MSA) and Progressive Supranuclear Palsy (PSP), while vascular Parkinson’s is caused by small strokes.
Here’s a more detailed breakdown:
Atypical Parkinson’s:
- Causes:
A diverse group of neurodegenerative disorders, including MSA and PSP, that share some Parkinsonian features but have unique clinical and pathological characteristics.
- Progression:
Often progresses more rapidly than Parkinson’s disease, with early functional decline, gait impairment, and falls.
- Treatment:
Typically does not respond well to levodopa, a common medication for Parkinson’s disease.
- Examples:
Multiple System Atrophy (MSA): Characterized by parkinsonian symptoms, autonomic dysfunction (e.g., blood pressure instability), and cerebellar dysfunction (e.g., balance problems).
Progressive Supranuclear Palsy (PSP):** Presents with parkinsonism, eye movement abnormalities (e.g., difficulty looking up or down), and cognitive difficulties.
Diagnosis:**
Can be challenging due to overlapping symptoms and lack of specific biomarkers, often requiring a combination of clinical assessment, neuroimaging (MRI, PET scans), and, in some cases, post-mortem examination.
Vascular Parkinson’s (Multi-Infarct Parkinsonism):
Cause:**
Caused by small strokes (brain infarcts) affecting blood supply to the brain, leading to Parkinsonian symptoms.
Progression:**
Can be relatively slow, with symptoms potentially worsening over time if more strokes occur.
Treatment:**
May respond less effectively to levodopa than typical Parkinson’s disease.
Symptoms:**
Often presents with lower body parkinsonism (more prominent symptoms in the legs), walking difficulties, and balance problems.
Diagnosis:**
Can be suspected based on the presence of small strokes on brain imaging (MRI) and a history of vascular risk factors.
Best wishes
Steve2