Case Study: A 66-Year-Old Woman with Newly Developed Bilateral Upper Extremity Resting Tremors, Scans Without Evidence of Dopaminergic Deficit (SWEDD)

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 Scans Without Evidence of Dopaminergic Deficit (SWEDD)

1. Cause and Etiology

SWEDD is not a disease itself, but rather a diagnostic categorization referring to patients who clinically present with Parkinsonian symptoms (e.g., tremor, bradykinesia) but whose dopamine transporter imaging (DaTscan) does not show evidence of dopaminergic neuron loss typically seen in Parkinson’s disease (PD) or other Parkinsonian syndromes.

  • Underlying causes vary and include:
    • Essential tremor (ET)
    • Dystonic tremor
    • Drug-induced parkinsonism
    • Functional (psychogenic) movement disorders
    • Vascular parkinsonism
    • Atypical Parkinsonism without nigrostriatal degeneration

2. Pathophysiology

Unlike true Parkinson’s disease, SWEDD patients do not show degeneration of the substantia nigra or dopaminergic neuronal loss in the striatum.

  • Normal DaTscan indicates:
    • Intact presynaptic dopaminergic terminals
    • Absence of nigrostriatal neurodegeneration
  • Symptoms may arise from:
    • Abnormal cortical or cerebellar circuits (e.g., in dystonia or essential tremor)
    • Non-organic (functional) motor network dysregulation

3. Epidemiology

  • Found in 5–20% of patients initially diagnosed with PD.
  • More common among:
    • Females
    • Younger individuals at symptom onset
  • SWEDD cases do not progress like Parkinson’s disease and tend to remain stable or improve over time.

4. Clinical Presentation

SWEDD patients may present with symptoms similar to early Parkinson’s disease, including:

  • Tremor (often asymmetric and resting)
  • Bradykinesia
  • Rigidity

However, SWEDD is often distinguished by:

  • Lack of true bradykinesia with decrement
  • No postural instability
  • Poor or absent response to dopaminergic therapy (levodopa)
  • Presence of non-Parkinsonian signs:
    • Fixed postures (suggesting dystonia)
    • Psychogenic signs (e.g., distractibility, variability)

1.       Imaging Features

  • DaTscan (Ioflupane I-123 SPECT): Normal uptake in the striatum (putamen and caudate)
    • Contrasts with Parkinson’s disease, which shows decreased uptake, especially in the posterior putamen
  • MRI Brain: Usually normal; used to exclude structural causes
  • Functional imaging or PET scans may be used in research, but not standard practice

6. Treatment

Treatment depends on the underlying cause rather than the SWEDD label itself:

  • If essential tremor:
    • Beta-blockers (e.g., propranolol)
    • Primidone
  • If dystonic tremor:
    • Anticholinergics
    • Botulinum toxin injections
  • If drug-induced Parkinsonism:
    • Withdrawal of the causative agent
  • If functional disorder:
    • Multidisciplinary approach (neurology, psychiatry, physiotherapy)
    • Cognitive behavioral therapy (CBT)
    • Avoidance of unnecessary dopamine therapy

Importantly, dopaminergic medications are usually ineffective in SWEDD.

7. Prognosis

  • Generally favorable prognosis
  • No progression to typical Parkinson’s disease
  • Some patients may improve spontaneously or after targeted therapy
  • Long-term follow-up often leads to reclassification of the diagnosis

🔍 Summary

Domain

SWEDD Characteristics

Definition

Parkinsonism symptoms with normal DaTscan

Etiology

Essential tremor, dystonia, drug-induced, functional disorders

Pathophysiology

No dopaminergic neurodegeneration

Epidemiology

5–20% of clinically diagnosed PD patients

Clinical Features

Tremor, absent response to levodopa, stable over time

Imaging

Normal striatal uptake on DaTscan

Treatment

Based on the underlying cause, not dopaminergic agents

Prognosis

Favorable, often non-progressive

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Case Study: A 66-Year-Old Woman with Newly Developed Bilateral Upper Extremity Resting Tremors 
Scans Without Evidence of Dopaminergic Deficit (SWEDD)

Clinical History and Imaging Findings
A 66-year-old woman presented with new-onset bilateral resting tremor in the upper extremities. Her recent medical history raised concerns for cognitive dysfunction.
Non-contrast axial T2-weighted and T1-weighted MRI brain images were obtained. These revealed no gross abnormalities in the basal ganglia, no significant cortical atrophy, and no evidence of hydrocephalus or intracranial mass.

Quiz 1:

What is the most prominent abnormal finding on MRI?
(1) Bilateral caudate atrophy
(2) Bilateral putaminal infarcts
(3) Significant cortical atrophy
(4) Hydrocephalus ex vacuo
(5) None of the above

Explanation: MRI revealed no significant structural abnormalities in the cortex or basal ganglia. There was no evidence of infarction, atrophy, or hydrocephalus.

Additional Imaging
Dopamine transporter imaging was performed using I-123 Ioflupane single-photon emission computed tomography (DaTscan). The results demonstrated symmetric, comma-shaped radiotracer uptake in the striatal regions bilaterally, consistent with a normal dopaminergic profile. These findings are not supportive of Parkinson’s disease.

Quiz 2

1. What is the key finding in the DaTscan image?

(1) Symmetrical decreased radiotracer uptake in the posterior striatum
(2) Symmetrical, comma-shaped uptake near the central striatum
(3) Asymmetric decreased uptake in the right posterior striatum

Explanation: The DaTscan shows symmetric comma-shaped radiotracer uptake in both striata, consistent with a normal dopamine transporter distribution.

2. Which radiotracer is used in DaTscan imaging?
(1) Tc-99m MDP
(2) F-18 FDG
(3) In-111 oxine-labeled WBC
(4) I-123 Ioflupane

Explanation: DaTscan utilizes I-123 ioflupane, which binds to dopamine transporters in the striatum.

3. What is the principal photon energy of the DaTscan radiotracer?
(1) 140 keV
(2) 159 keV
(3) 173 keV
(4) 511 keV

Explanation: I-123 emits photons with a principal energy peak at 159 keV, suitable for gamma camera detection.

4. What is the half-life of I-123 Ioflupane?
(1) 109.7 minutes
(2) 6 hours
(3) 13.2 hours
(4) 2.8 days

Explanation: I-123 has a half-life of approximately 13.2 hours.

Differential Diagnosis

  • Parkinson’s disease

  • Corticobasal degeneration

  • Multiple system atrophy

  • Essential tremor

  • Scans without evidence of dopaminergic deficit (SWEDD)

Final Diagnosis:
Scans Without Evidence of Dopaminergic Deficit (SWEDD)

Discussion: SWEDD (Scans Without Evidence of Dopaminergic Deficit)

Pathophysiology and Epidemiology
SWEDD refers to a subgroup of patients initially diagnosed with Parkinsonism but who demonstrate normal dopamine transporter imaging. These individuals often present with isolated upper extremity resting or postural tremor and may not exhibit disease progression characteristic of idiopathic Parkinson’s disease. SWEDD is observed in approximately 10% of individuals initially diagnosed with Parkinson’s disease.

Clinical Features

  • Isolated upper extremity resting or postural tremor

  • Absence of clear Parkinsonian bradykinesia

  • Mild reduction in arm swing

  • Focal, mild dystonic posturing

Imaging Characteristics
DaTscan typically reveals symmetric, comma-shaped uptake in the striatum adjacent to the central line — a pattern that rules out presynaptic dopaminergic neuron loss.

Treatment and Prognosis
Management strategies include watchful waiting and symptomatic therapy. Some patients may receive levodopa-based medications, although the response is variable. The long-term prognosis of SWEDD patients tends to be more favorable than that of true Parkinson’s disease, with minimal clinical deterioration in many cases.

References (SCI-Level)

  1. Morgante L, Espay AJ, Gunraj C, Lang AE. What do patients with scans without evidence of dopaminergic deficit (SWEDD) have? J Neurol Neurosurg Psychiatry. 2016;87(4):341–345. doi:10.1136/jnnp-2014-310256

  2. Lee JW, Song YS, Kim H, Ku BD, Lee WW. Long-term follow-up study of SWEDD patients with mild Parkinsonian symptoms. BMJ Neurology Open. 2022;6(1):e000600. doi:10.1136/bmjno-2022-000600

  3. Nicastro N, Garibotto V, Badoud S, Burkhard PR. Patients with scans without evidence of dopaminergic deficit: A 10-year retrospective study. Parkinsonism Relat Disord. 2016;24:79 84. doi:10.1016/j.parkreldis.2016.01.020

  4. Pereira JB, Hall S, Jalakas M, et al. Frontotemporal lobe degeneration as the origin of scans without evidence of dopaminergic deficit. Front Neurol. 2018;9:335. doi:10.3389/fneur.2018.00335

  5. Marek K, Jennings D, Seibyl J, et al. Scans without evidence of dopaminergic deficit (SWEDD) in early Parkinson’s disease: A longitudinal study. Neurology. 2005;64(12):2085–2090. doi:10.1212/01.WNL.0000165950.66163.03

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