Abstract - Do Robotics Really Help in Parkinson’s Rehabilitation? Meta-Analysis Reveals Modest Gains

Title: Do Robotics Really Help in Parkinson’s Rehabilitation? Meta-Analysis Reveals Modest Gains

Authors: Ana Leticia Fornari Caprara, Jamir Pitton Rissardo, and Ian M. Walker

Conference: 2026 MDS-PAS, Houston, TX
 
Objective
To evaluate the effects of robot‑assisted rehabilitation on motor symptoms and functional mobility in Parkinson’s disease (PD).

Background
Robotic technologies are increasingly used to enhance gait and balance training in PD, but their clinical benefit remains uncertain.

Design/Methods
Randomized controlled trials comparing robot‑assisted versus conventional therapy in PD were analyzed. Outcomes (ON‑medication) included UPDRS‑III, UPDRS‑Total, Timed Up and Go (TUG), 6‑Minute Walk Test (6‑MWT), 10‑Meter Walk Test (10‑MWT), and Berg Balance Scale (BBS). Pooled mean differences (MD) or standardized mean differences (SMD) with 95% confidence intervals were calculated using random‑effects models; heterogeneity was assessed with I2.

Results
Robot‑assisted training demonstrated limited to modest effects compared with controls. For UPDRS‑III (ON), the pooled MD was 0.35 (95% CI –1.06 to 1.76; I² = 0%), indicating no significant motor benefit. UPDRS‑Total (ON) favored robotics with an MD of –3.72 (95% CI –5.65 to –1.79; I² = 30%), suggesting a small but statistically significant improvement in overall motor disability. Functional outcomes showed mixed results: TUG had a SMD of 0.13 (95% CI –0.14 to 0.41; I² = 55%), and 10‑MWT showed an SMD of 0.24 (95% CI –0.05 to 0.53; I² = 84%), both indicating small, non‑significant gains with moderate to high heterogeneity. 6‑MWT effects (SMD 0.07; 95% CI –0.24 to 0.38; I² = 91%) and BBS changes (MD 0.45; 95% CI –0.36 to 1.26; I² = 0%) were non-significant.

Conclusions
Robot-assisted rehabilitation provides a small but significant improvement in UPDRS-Total, while showing no meaningful effect on UPDRS-III or functional outcomes (TUG, 6-MWT, 10-MWT, BBS). High heterogeneity in gait measures suggests variability in devices, protocols, and patient characteristics.

Citation
Caprara ALF, Rissardo JP, Walker I. Do Robotics Really Help in Parkinson’s Rehabilitation? Meta-Analysis Reveals Modest Gains. Mov Disord Clin Pract 2026;13(S1):S100–S101. doi: 10.1002/mdc3.7047.
Figure 1. Forest plots showing pooled effects of robotic rehabilitation on UPDRS‑III (ON), UPDRS‑Total (ON), TUG, 6‑MWT, 10‑MWT, and BBS outcomes.

Abstract - GLP-1 Receptor Agonists for Motor and Non-Motor Outcomes in Parkinson’s Disease: A Systematic Review and Meta-Analysis

Title: Effects of Yoga on Motor and Non-Motor Symptoms in Parkinson’s Disease: A Systematic Review and Meta-Analysis

Authors: Ana Leticia Fornari Caprara, Jamir Pitton Rissardo, and Ian M. Walker

Conference: 2026 MDS-PAS, Houston, TX

Objective
To assess the impact of GLP-1 receptor agonists on motor and non-motor symptoms in Parkinson’s disease (PD).

Background
GLP-1 receptor agonists, originally developed for diabetes, have shown neuroprotective effects in preclinical PD models. Clinical trials have explored their potential to improve motor and non-motor outcomes, but findings remain inconsistent.

Design/Methods
We systematically reviewed randomized controlled trials (RCTs) comparing GLP-1 receptor agonists (exenatide, liraglutide, lixisenatide, NLY01) with placebo or standard care in PD. Primary outcomes were changes in Unified Parkinson’s Disease Rating Scale part III (UPDRS-III) in ON and OFF medication states; non-motor symptoms (NMS) were secondary. Mean differences (MD) with 95% confidence intervals (CI) were pooled using fixed-effect and random-effects models.

Results
Five trials (n.E. 258 and n.C. 239) were included. GLP-1 receptor agonists significantly improved UPDRS-III in the ON state (pooled MD fixed-effect –2.40, 95% CI –3.89 to –0.91; random-effect –2.53, 95% CI –5.01 to –0.06), indicating a meaningful benefit, with moderate heterogeneity (I2 59.3%). Also, a significant effect was observed in the OFF state (pooled MD fixed-effect –1.19, 95% CI –2.34 to –0.04), and heterogeneity was moderate (I2 56.2%). For NMS, the effect was negligible (pooled fixed-effect MD 0.11, 95% CI –2.61 to 2.83; I2 42.4%).

Conclusions
GLP-1 receptor agonists may provide motor benefits in the ON and OFF medication states but show no clear advantage for non-motor symptoms. Moderate to high heterogeneity and limited sample sizes warrant cautious interpretation. Larger, longer-duration trials are needed to confirm potential disease-modifying effects.

Citation
Caprara ALF, Rissardo JP, Walker I. GLP-1 Receptor Agonists for Motor and Non-Motor Outcomes in Parkinson’s Disease: A Systematic Review and Meta-Analysis. Mov Disord Clin Pract 2026;13(S1):S99–S100. doi: 10.1002/mdc3.7047.
Figure 1. Forest plots showing pooled effects of GLP‑1 receptor agonists on UPDRS‑III ON, UPDRS‑III OFF, and NMSS outcomes across medication subgroups, with mean differences and 95% confidence intervals.

Abstract - Effects of Yoga on Motor and Non-Motor Symptoms in Parkinson’s Disease: A Systematic Review and Meta-Analysis

Title: Effects of Yoga on Motor and Non-Motor Symptoms in Parkinson’s Disease: A Systematic Review and Meta-Analysis

Authors: Ana Leticia Fornari Caprara, Jamir Pitton Rissardo, and Ian M. Walker

Conference: 2026 MDS-PAS, Houston, TX

Objective
To determine the impact of yoga interventions on motor and non-motor symptoms in individuals with Parkinson’s disease (PD).

Background
Yoga, a mind-body practice combining specific body postures, breathing exercises, and mindfulness, has been proposed as an adjunct therapy for PD. While individual trials suggest benefits for motor function and psychological well-being, pooled evidence remains limited.

Design/Methods
We systematically searched major databases (PubMed and Google Scholar) for randomized controlled trials comparing yoga to control interventions in PD. Eligible studies reported changes in motor symptoms (UPDRS-III), balance (Mini-BEST, BBS), freezing of gait (FOG), and psychological outcomes (BAI, HADS-anxiety, HADS-depression). Standardized mean differences (SMD)  and mean differences (MD) with 95% confidence intervals were calculated using fixed-effect and random-effect models.

Results
Six trials (174 n.E. and n.C 166) met inclusion criteria. Yoga significantly improved motor symptoms [UPDRS-III: MD fixed-effect –3.80 (95% CI: –5.28; –2.33) and random-effect –3.87 (95% CI: –5.44; –2.29); I2 1.5%] and balance [BBS: MD 3.8 (95% CI: 2.19; 5.41)] inconsistently [Mini-BEST: MD 1.98 (95% CI: –0.13; 4.09); I2 0%]. Freezing of gait showed no significant improvement [MD –0.93 (95% CI: –3.52; 1.6)]. For psychological outcomes, yoga was associated with mild reductions in depression [HADS-depression: MD –0.92 (95% CI: –1.43; –0.40); I2 84%]; though anxiety [HADS-anxiety: MD –0.49 (95% CI: –0.99; 0.02); I2 83%] and BAI [SMD –0.52 (95% CI:  –1.11; 0.07); I2 85%] results were inconsistent. Heterogeneity was low to high, likely due to differences in yoga practices, session frequency and duration, and disease severity.

Conclusions
Yoga provides clinically meaningful improvements in motor function and balance and may reduce anxiety and depression in PD. These findings support yoga as a safe, accessible adjunct to standard care. Future research should standardize intervention protocols and assess long-term sustainability.

Citation
Caprara ALF, Rissardo JP, Walker I. Effects of Yoga on Motor and Non-Motor Symptoms in Parkinson’s Disease: A Systematic Review and Meta-Analysis. Mov Disord Clin Pract 2026;13(S1):S97–S98. doi: 10.1002/mdc3.7047.
Figure 1. Forest plots showing pooled effects of yoga interventions on UPDRS-III, Mini-BEST, HADS-Anxiety, HADS-Depression, and BAI outcomes, with mean differences and 95% confidence intervals.

Abstract - Treadmill Training Improves Motor and Balance Outcomes in Parkinson’s Disease: A Systematic Review of Randomized Controlled Trials

Title: Treadmill Training Improves Motor and Balance Outcomes in Parkinson’s Disease: A Systematic Review of Randomized Controlled Trials

Authors: Jamir Pitton Rissardo, Ana Leticia Fornari Caprara, and Ian M. Walker

Conference: 2026 MDS-PAS, Houston, TX

Objective
To systematically review randomized controlled trials (RCTs) evaluating the effects of treadmill training (TT) on motor symptoms, gait, functional mobility, and quality of life in Parkinson’s disease.

Background
Gait impairment and reduced mobility are major contributors to disability in Parkinson’s disease. Treadmill training has been proposed as a targeted intervention to improve walking performance and motor function, but its efficacy across clinical outcomes remains uncertain.

Design/Methods
A systematic search of PubMed was conducted to identify randomized controlled trials (RCTs) evaluating treadmill training (TT) in individuals with Parkinson’s disease. Eligible studies compared TT with conventional physiotherapy in adults diagnosed with Parkinson’s disease. Primary outcomes included motor symptoms (UPDRS-III), gait speed, stride length, functional mobility (Timed Up and Go [TUG]), walking capacity (6-Minute Walk Test [6MWT]), and quality of life (PDQ-39). Data were pooled using mean difference (MD) or standardized mean difference (SMD) with corresponding 95% confidence intervals (CI). Statistical heterogeneity was assessed using the I².

Results
Seven RCTs were included. TT significantly improved motor symptoms (UPDRS-III ON: MD −1.47; 95% CI −2.72 to −0.22; I² = 0%) and balance (BBS: MD 3.61; 95% CI 1.90 to 5.32; I² = 96%). Functional mobility showed a small, non-significant effect (TUG: SMD −0.35; 95% CI −0.95 to 0.25; I² = 0%). Walking capacity improvements were modest and not statistically significant (6MWT: SMD 0.34; 95% CI −0.32 to 0.99; I² = 49%). Quality-of-life changes were minimal (PDQ-39: MD −1.88; 95% CI −7.97 to 4.22; I² = 0%). TT was generally safe, with low dropout rates and minimal adverse events.

Conclusions
Treadmill training provides significant benefits for motor symptoms and balance in PD, with uncertain effects on functional mobility, walking capacity, and quality of life. Incorporating TT into multimodal rehabilitation programs may enhance outcomes.

Citation
Rissardo JP, Caprara ALF, Walker I. Treadmill Training Improves Motor and Balance Outcomes in Parkinson’s Disease: A Systematic Review of Randomized Controlled Trials. Mov Disord Clin Pract 2026;13(S1):S97–S98. doi: 10.1002/mdc3.7047.
Figure 1. Forest plots showing pooled effects of interventions on UPDRS‑III (ON), TUG, BBS, 6‑MWT, and PDQ‑39 outcomes across included studies.

Abstract - Bidirectional Association Between Parkinson's Disease and Skin Cancer: A Systematic Review and Meta-Analysis

Title: Bidirectional Association Between Parkinson's Disease and Skin Cancer: A Systematic Review and Meta-Analysis

Authors: Jamir Pitton Rissardo, Ana Leticia Fornari Caprara, and Ian M. Walker

Conference: 2026 MDS-PAS, Houston, TX

Objective
To quantify the bidirectional association between Parkinson’s disease (PD) and skin cancers, including melanoma and non-melanoma skin cancer (NMSC), and to explore subgroup differences.

Background
Observational studies suggest a link between PD and melanoma, but the magnitude, directionality, and influence of subgroups remain unclear.

Design/Methods
We systematically reviewed PubMed-indexed observational studies reporting melanoma or NMSC occurrence in PD patients or vice versa. Pooled effect sizes were calculated using fixed- and random-effects models, and heterogeneity was assessed with τ² and I². Most included studies were case-control designs, and results are summarized as risk ratios (RR).

Results
Thirty-one studies were included. For melanoma preceding PD, the random-effect estimate was 1.34 (95% CI, 1.02–1.78). For PD preceding melanoma, the random-effect estimate was 1.45 (0.98–2.13). For NMSC preceding PD, the estimate was 0.9 (0.71–1.14). When analyzed by cancer type, melanoma overall (22 studies) showed a random-effects estimate of 1.48 (1.15–1.91). NMSC overall (10 studies) showed a fixed-effect estimate of 1.15 (0.73–1.81). Gender-specific estimates from single studies were as follows: melanoma in males 2.75 (0.25–30.10), melanoma in females 0.69 (0.06–7.52), NMSC in males 0.93 (0.59–1.46), and NMSC in females 1.18 (0.56–2.47).

Conclusions
PD and melanoma demonstrate a consistent bidirectional association with low heterogeneity. Evidence for NMSC and gender-specific effects is limited and inconclusive.

Citation
Rissardo JP, Caprara ALF, Walker I. Bidirectional Association Between Parkinson's Disease and Skin Cancer: A Systematic Review and Meta-Analysis. Mov Disord Clin Pract 2026;13(S1):S68. doi: 10.1002/mdc3.7047.
Figure 1. Scatterplot of standardized treatment effects against inverse standard error, with regression line illustrating the relationship between study precision and effect magnitude.
Figure 2. L’Abbé plot showing experimental versus control event rates with study‑size weighting and fitted treatment‑effect trend lines
Figure 3. Contour‑enhanced funnel plot illustrating study effect sizes, confidence regions, and fixed‑ and random‑effects model estimates.

Abstract - Diabetes and Parkinson's Disease: A Hazard Ratio Meta-Analysis with Global and Sex-Specific Projections to 2050

Title: Diabetes and Parkinson's Disease: A Hazard Ratio Meta-Analysis with Global and Sex-Specific Projections to 2050

Authors: Jamir Pitton Rissardo, Ana Leticia Fornari Caprara, and Ian M. Walker

Conference: 2026 MDS-PAS, Houston, TX

Objective
To estimate Parkinson’s disease (PD) risk in individuals with diabetes mellitus (DM) using hazard ratios (HRs) from population-based studies and assess variation by sex, region, and diabetes type.

Background
DM and PD may share mechanisms such as insulin resistance and neuroinflammation, but the magnitude and consistency of this association remain unclear.

Design/Methods: A systematic review and meta-analysis of population-based cohort studies reporting HRs for PD among individuals with DM. Eligible studies used time-to-event models (Cox regression) and provided subgroup data by region (Asia, Europe, America), sex, and diabetes type (T1DM, T2DM, PreDM). Random-effects meta-analysis (DerSimonian-Laird) was applied. Publication bias was assessed via trim-and-fill and fail-safe N. Sex-specific projections of PD cases attributable to DM (2025–2050) were modeled using normalized population data and linear growth assumptions.

Results
Thirty studies were included. Pooled log(HR) for PD in DM was 1.29 (95% CI: 1.21–1.37), with a prediction interval of 0.85–1.72. Regional estimates: Asia 1.25 (1.08–1.42), Europe 1.37 (1.08–1.66), America 1.17 (1.11–1.22). Sex-specific log(HRs) were higher in women [1.41 (1.26–1.56)] than men [1.25 (1.10–1.41)] in European cohorts. By diabetes type, T2DM showed the strongest association [log(HR) 1.17–1.42], PreDM had a smaller effect (1.01–1.29), and T1DM was based on one study [1.38 (0.86–1.90)]. Heterogeneity was low (I² < 1%). Publication bias was minimal (adjusted log(HR) 1.36; fail-safe N > 11,000). Projections showed PD cases attributable to DM increasing from 12.3 to 21.4 per 100,000 in Asia, 15.1 to 24.8 in Europe, and 10.7 to 18.2 in America by 2050, with steeper increases in women.

Conclusion
Diabetes is associated with a modest but significant increase in PD risk, varying by geographic distribution, sex, and diabetes type. Using log(HRs) provides time-dependent insights, enhancing clinical relevance for risk stratification.

Citation
Rissardo JP, Caprara ALF, Walker I. Diabetes and Parkinson's Disease: A Hazard Ratio Meta-Analysis with Global and Sex-Specific Projections to 2050. Mov Disord Clin Pract 2026;13(S1):S67–S68. doi: 10.1002/mdc3.7047.
Figure 1. Forest plot showing pooled hazard ratios linking T2DM to Parkinson’s disease across Asian, European, and American cohorts, with subgroup and overall fixed‑effect estimates
Figure 2. Forest plot comparing hazard ratios for Parkinson’s disease in men and women with T2DM across Europe and Asia, showing subgroup and overall fixed‑effect estimates.
Figure 3. Forest plot showing pooled hazard ratios for Parkinson’s disease in prediabetes and type 1 diabetes across Asian and European cohorts, including subgroup and overall fixed‑effect estimates.
Figure 4. Funnel plot with confidence contours and Egger regression assessing publication bias across included studies examining diabetes and Parkinson’s disease, showing effect‑size symmetry and small‑study effects.
Figure 5. Projected Parkinson’s disease cases attributable to T2DM, T1DM, and prediabetes from 2025–2050 across Asia, Europe, and America, normalized per 100,000 population.
Figure 6. Projected Parkinson’s disease cases attributable to T2DM, T1DM, and prediabetes by sex from 2025–2050 across Asia, Europe, and America, normalized per 100,000 population.

Dizziness

Dizziness
David Newman-Toker, neuro-otology
Senior author of "HINTS to diagnose stroke"

What is dizziness?
-Dizziness→ impaired perception of spatial orientation without vertigo
-Vertigo→ illusion of motion (spinning/non-spinning)
>Subjective (person)→ MC peripheral
>Objective (environment)→ MC central
-Oscillopsia 'world bounces'
>can’t read signs while walking
>B/L vestibular hypofunction
-Lightheadness, syncope→ LOC
-Imbalance→ severe truncal ataxia

Red flags associated sx
-Headache→ new
-Neck pain→ dissection
-AMS→ toxic
-CP→ PE & MI

Dizziness Ddx
“If you are sitting still with your eyes closed, are you still dizzy?”
Y→ Acute (Continuous) Vestibular Syndrome
N→ Episodic Vestibular Syndrome
Triggers
Positional, orthostatic, motion, auditory, visual, dietary
BPPV
-Position‑change + Short + Intense + Torsional
-Hx of TBI
-3-types
>Posterior→ vertical + MC BPPV + typical torsional nystagmus
>Horizontal→ lateral + turning + geotropic/apogeotropic nystagmus
>Superior→ vertical + rare + downbeat torsional pattern

Middle ear disease (otitis/effusion)
-Otalgia
-Does not produce vertigo, but sense of imbalance
-Rare syphilis

Vestibular neuritis ≠ labyrinthitis
-Neuritis→ No hearing loss; labyrinthitis→ Y
-DDx: Neuritis→ PICA; Labyrinthitis→ AICA
-Post-viral, self-resolution wks-mo

Meniere disease
-VERT→ Vertigo (recurrent); Ear fullness (pressure); Ringing (tinnitus); Thump/low-tone hearing loss
-2015 Barany criteria→ ≥2 spontaneous vertigo episodes 20 min–12 hr

Vestibular migraine
-Episodic dizziness + migraine features + motion sensitivity + no hearing loss
-NOT req headache, and headache may come before, during, or after the vertigo

Persistent Postural‑Perceptual Dizziness (PPPD)
-Chronic + worse with motion/visual stimuli + triggered by a past event + normal exam
-Grows out when another problem ends (PMH of VN, BPPV, VM, TBI, psych)

Medications
-CALM EAR→ Cisplatin, Aminoglicoside, Loop diuretics, Malaria; Erythromycin, Asa, Redman (vancomycin)
-Others: taxane, bevacizumab

Perilymphatic Fistula (PLF) and Superior Canal Dehiscence (SCD)
-PLF→ sudden hearing loss + pressure-triggered vertigo after trauma
-SCD→ conductive hearing loss + sound-triggered vertigo + autophony

Carotid‑Cavernous Fistula (CCF)
-Pulsatile tinnitus + red eye + diplopia
-DSA

Acoustic neuroma
-U/L hearing loss + U/L tinnitus + chronic imbalance (not vertigo)
>CPA→ facial numbness
-NF2

VBI
-Vertigo + brainstem signs (diplopia/dysarthria/ataxia) + no hearing loss
-Sx occur at rest, NOT positional
≠Bow Hunter→ triggered ONLY by head rotation
>Dynamic imaging showing mechanical compression
-CTA w/ post circ stenosis

Stroke syndromes assoc w/ dizziness
-Hearing loss→ AICA
-Sensory→ Thalamus
-Vision→ PCA
-Quadriplegia→ Basilar
Physical exam
-POC & T° & BP
-Otoscopy→ cerumen, infection
-OH BP + telemetry→ cardiac source
-HINTS→ only w/ dizzy or nystagmus
>HINTS (SN100) vs MRI[<48h](SN88)→ to dx post circ stroke
>HINTS-plus→ add hearing test eval
-Cerebellar signs
-Gait
-Dix-Hillpike→ episodic and triggered by head movement
>Roll test→ positional, but Dix-Hillpike
-Romberg Test
-Fukuda test

HI-N-TS & IN-FA-RCT
Impulse Normal
Fast-phase Alternating
Refix on Cover Test
Head-Impulse
-Abnormal→ peripheral; Abnormal→ good
-Normal is absence of saccades
Nystagmus
-Horizontal-Torsional and unidirectional
-Look at other side decrease (Alexander's law)
Test of Skew
-No vertical skew
≠CN IV
Dix–Hallpike
Maneuver
Positive Dix Hallpike
Roll test
-Vertigo is positional, BUT ⊖Dix‑Hallpike
-Nystagmus looks horizontal
-Sx triggered by rolling in bed
-Suspect horizontal canal BPPV (geo = affected; apo = unaffected)
Romberg test
→ verstibular dysf or sensory (peripheral neuropathy, post column disease)
*Sharpened (Tandem) Romberg test→ feet in tandem + arms crossed
Fukuda (Unterberger) test
-Marches in place, 50 steps
-Do: chronic imbalance; suspected unilateral vestibular loss
-Positive: ≥30° rotation→ peripheral vestibular weakness
Investigation
Labs
CBC→ sev anemia, infection
CMP→ all associated w/ dizziness/imbalance
POC→ hypo/hperG

Others: 
A1c, OGTT, lipid profile (triglycerides), TSH, vit (B12 & D)
Lyme titers→ if vertigo + cranial neuropathies
HIV/RPR→ if encephalopathy, neuropathy, or atypical findings
Cardiac markers→ troponin, BNP
UDS + alcohol level

ILR/MCOT→ recurrent events
+/-routine-EEG

Neuroimaging
If classic BPPV→ no need; otherwise→ do it

Acute→ CTH & CTA H&N→ post circ infarcts & stenosis
bMRI D/H→ c/f central etiology
IAC-MRI→ U/L SNHL, U/L tinnitus
CT Temporal bone→ PLF, SCD, temporal bone trauma

Audiometry→ hearing loss, tinnitus, aural fullness, unexplained vertigo

Treatment
-NO long-term vestibular sedation→ blocks recovery
-General (vestibular sedatives)
>Meclizine PO 25q8
>Diphenhydramine PO/IV 25q8;
>Scopolamine TD 1.5q3d behind ear
>Diazepam 2q8 or lorazepam 0.5q8
-Medrol dose pack
-Vestibular rehabilitation therapy

VNeuritis/Labyrinthitis
<72h→ pred 60q24 for 5d
-Vestibular sedative→ meclizine

Meniere disease
-Low‑salt diet
-Limit caffeine/alcohol
-Thiazide‑type diuretics→ HCTZ 25q24
-Betahistine (no USA 2/2 lack efficacy)
-Steroids (intratympanic or PO) for flare‑ups
-ENT referral for refractory cases:
>Intratympanic gentamicin (caution: hearing risk)
>Endolymphatic sac decompression

Vestibular migraine
-Treat migraine

PPPD, Anxiety‑Related Dizziness
-SSRIs/SNRIs (sertraline/venlafaxine)
-CBT
>If anxiety, breathing techniques
-Treat underlying vestibular event that triggered PPPD

BPPV
-Reposition→ Epley, Semont, Gufoni
-Teach home Epley if recurrence

Epley maneuver
-Worse sx→ consider, sedative
-Rotate 1st to affected side
-Steps: 1) Turn head 45° toward affected ear. 2) Lie back into Dix Hallpike position. 3) Wait for symptoms to stop. 4) Turn head 90° to the opposite side. 5) Roll onto side (nose toward floor). 6) Sit up slowly
Home Epley
Semont maneuver
-Rotate 1st to non-affected side
-Steps: 1) Turn head 45° away from affected ear. 2) Drop rapidly to affected ear down side. 3) Hold 1 minute. 4) In one motion, swing to opposite side. 5) Hold 1 minute. 6) Sit up
Foster (Half‑Somersault)
-Steps: 1) Kneel and place head on floor. 2) Turn head 45° toward affected ear. 3) Lift head halfway (back straight). 4) Sit up
BBQ Roll (Lempert)
-Rotate 1st to affected side
-Steps: 1) Lie on back with head flexed 30°. 2) Turn head 90° toward affected side. 3) Turn head to midline. 4) Turn head 90° to opposite side. 5) Roll body onto stomach (face down). 6) Roll onto side and sit up
Gufoni
-Steps: 1) Sit upright. 2) Fall quickly to unaffected side. 3) After 1 min, turn head 45° downward. 4) Hold 2 min. 5) Sit up
-Appiani is when fall to affected side
Casani
Zuma‑e‑Maia
Yacovino
-Steps: 1) Sit upright. 2) Move quickly to head hanging supine position. 3) Hold 30 seconds. 4) Bring head up to chin to chest. 5) Sit up

227. Accepted

Mirror Movements

Mirror Movements (Spiegelschrift)
1st described by Dr. Friedrich Albrecht Erlenmeyer (1849–1926)
Grundzüge ihrer Physiologie und Pathologie, 1879

Definition
"Involuntary movements on one side that mirror voluntary actions on the other"
-Normal in <7–10yo (CC myelination), 70% healthy children (on speed-based task)

Pathophysiology
Three teories
-Overflow
> signal 'overflows' to the other hand 
-Weak interhemispheric inhibition
> both hemispheres fire together
-Abnormal crossing motor pathways
>same commands go to both hands
Key quests
-Development & family history
-Cognitive & neuropsych

Exam
-Rapidly finger‑tap, open/close the fist, or perform pronation-supination
>MC in UEs
>Watch the “quiet” hand

-Woods & Teuber scale
0→ none
1→ barely
2→ clear, mod amplitude (<50%); 2a (slight) & 2b (strong)
3→ clear, large amplitude (>50%)
4→ complete, unable to supress
W&T=0
No clear imitative movements. Right hand is active and left hand is scored
W&T=1
Barely discernible repetitive movements. Right hand is active and left hand is scored
W&T=2a
Slight mirror movements. Right hand is active and left hand is scored
W&T=2b
Stronger, but briefer, repetitive movements. Right hand is active and left hand is scored
W&T=3
Strong and sustained repetitive movements. Left hand is active and right hand is scored
W&T=4
Movements equal to those observed in the active hand. Left hand is active and right hand is scored
Diagnostic work-up
-Affect QoL, otherwise no need
>Children unable to climb a ladder because releasing one hand makes the other involuntarily release too
>Painful compensatory shoulder contractions while writing
-Adults→ secondary (affecting CST)
>normal: fatigue, stress, high cognitive load, and aging
>investigate, if new in adulthood

Electrophysiology
-TMS
>Patho: simultaneous response & normal latency
>Physio: delayed responses & longer latency
-EMG: synchronous recruitment of homologous muscle groups, often with near‑identical timing to the voluntary contraction
-CMM demonstrates coactivation without delay

Neuroimaging
-bMRI to evalaute CC
>DTI→ ↓FA CC
>Asymmetric sigmoid bundle
-fMRI→ resting‑state   
-c-spine MRI
>spine abnormality
>vertebral fusion→ KFS

Genetic
-DCC (>80% of cases), followed by RAD51, NTN1, and ARHGEF7

Clinical Pearls
MM vs synkinesias
-Synkinesia→ no mirror

MM vs Imitation
-Imitation→ frontal lobe disinhibition (≠ behavior)

MM vs affected hand
-PD→ less affected hand
-CBS/CJD→ more affected hand
*MM co-exist w/ alien hand phenomenon: early (CJD) vs late (CBS)
-ET→ either
-HD→ UHDRS TMS correlated w/ MM

Treatment
-PT/OT→ bimanual independence, adpt at school/work
>HABIT-ILE→ CP-related MM
-Botox→ contralateral dystonia
-PD→ dopamine therapy adjustment
-Surgical→ no effect
-TMS→ research

Etiology
CMM
Mutations affecting CST
-DCC: req for CST axon guidance
-NTN1: chemoattractant for decussating CST axons
-RAD51: axonal migration & midline crossing indirectly
-ARHGEF7: cytoskeletal remodeling for CST

DCC
DCC
RAD51
PD
May precede motor asymmetry
-Asymmetric DA degeneration
-Loss of striato‑thalamo‑cortical regulation of motor suppression
-Inc motor overflow 2/2 impair inhibition

PD
PD
PD
-not really MM, but overflow
-RSM w/ mouth moves
LID


Others
-Focal hand dystonia
>if contralateral use, MM-dystonia 
>Botox contralateral
>Rare sensory coupling
-Klippel-Feil syndrome
#FND→ TMS
-Other craniovertebral anomalies
#KFS
-Kallmann syndrome
-Joubert syndrome
-Stroke
>R MCA territory infarct
>Limitation QoL
-CJD
-Tumor
>M1 resection
-KMT2B
Others
-ALS
-HD