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![• Family history. Patients with Mendelian pattern of inheritance
constitute a small minority of the overall Parkinson’s disease
(PD) population.
• Heritable disorders that can mimic PD include Wilson’s
disease (autosomal recessive [AR]), juvenile Huntington’s
disease (HD; autosomal dominant [AD]), and essential tremor
(ET; AD with variable penetrance).](https://image.slidesharecdn.com/approachtoparkinsonism-210721073643/75/Approach-to-parkinsonism-22-2048.jpg)
![Context-dependent laboratory exclusion criteria:
In patients with PSP-CBS, exclude primary Alzheimer disease pathology (typical
cerebrospinal fluid constellation [ie, both elevated total tau and phospho-tau
protein and reduced beta-amyloid 42] or pathological beta-amyloid PET imaging)
In patients <45 years of age, exclude:
• Wilson disease
• Niemann-Pick disease, type C
• Hypoparathyroidism
• Neuroacanthocytosis
• Neurosyphilis
In rapidly progressive patients, exclude:
• Prion disease
• Paraneoplastic encephalitis (anti-ma2, iglon-5)
In patients with suggestive features (ie, gastrointestinal symptoms, arthralgias, fever,
younger age, and atypical neurologic features such as myorhythmia), exclude
Whipple disease](https://image.slidesharecdn.com/approachtoparkinsonism-210721073643/75/Approach-to-parkinsonism-29-2048.jpg)
![IMAGING
Posterior putaminal atrophy with
marginal hyperintensity on T2.
Pontine atrophy with cross like
hperintensity, MCP atrophy and
atrophy of superior vermis.
FDG PET demonstrate
hypometabolism of putamen and
cerebellum
MSA
Atophy of midbrain and superior
cerebellar peduncle and dilation of
third ventricle. Mid-sagittal plane s/o
hummingbird sign and axial images
s/o morning glory sign.
FDG PET images show
hypometabolism in the posterior
frontal lobes and basal ganglia, worse
on the right side .
PSP
Asymmetric frontoparietal atrophy.
Hyperintensity in the subcortical
white matter in the rolandic region on
FLAIR images with asymmetric
atrophy in the cerebral peduncle, and
atrophy in the midbrain tegmentuM
PET scans show reduced
[18F]fluorodopa uptake in the
caudate and putamen and markedly
asymmetrical cortical
hypometabolism, especially in the
superior temporal and inferior
parietal lobe
CBD
h typical PD is usually normal;
but a high-field-strength (1.5 T)
heavily T2-weighted MRI may
show a wider area of lucency in
the SN
FDG PET image shows parietal
and strital hypometabolism
IPD](https://image.slidesharecdn.com/approachtoparkinsonism-210721073643/75/Approach-to-parkinsonism-76-2048.jpg)
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Approach to parkinsonism
- 1. APPROACH TO PARKINSONISM Dr. ShubhamGarg SR Neurology GMC Kota
- 2. INTRODUCTION • Term Parkinsonismis used to describe a syndrome manifested by a combination of the following six cardinal features: (1) tremor at rest, (2) bradykinesia, (3) rigidity, (4) loss of postural reflexes, (5) flexed posture, and (6) freezing (motor blocks). • Idiopathic Parkinson’s disease (IPD) is the most common cause of parkinsonism. Bradley's Neurology in Clinical Practice.2021.8th ed.
- 3.
- 5. Any approach beginswith . . . 1. A good history 2. A good physical exam 3. Keen sense of observation 4. A systematic differential diagnosis
- 6. Evaluation of Parkinsonism:History • Direct motor manifestations of parkinsonism: Bradykinesia, rest tremor, and rigidity especially if asymmetric with a postural imbalance in the absence of other neurologic complaints may suggest a diagnosis of IPD . • Association of hypokinesia/ bradykinesia with other neurologic symptoms usually suggests a condition other than IPD. • Another useful historical fact in differentiating IPD from other forms of parkinsonism is the sequence in which otherwise typical parkinsonian symptoms appear.
- 7.
- 8. Causes of hypokinesia(slowness of movement) Nonneurological 1. Poor eyesight 2. Joint problems 3. Depression, catatonia 4. Chronic diseases (cardiac, respiratory) Neurological 1. Spasticity 2. Cerebellar disorders 3. Peripheral neuropathy 4. Neuromuscular disorders 5. Muscle diseases Basal ganglia 1. Parkinson’s disease 2. Parkinson mimics
- 9. TREMOR UNILATERAL REST PD PSP-P INTENTION MSA-C POSTURAL/KINETIC MSA-P CBD BILATERAL POSTURAL+ FAMILY HISTORY ET REST+ INTENTION ENHANCED PHYSIOLOGICAL TREMOR MISCELLANEOUS PILLROLLING-PD JERKY-MSA,CBD WING BEATING-WD RUBRAL-VP
- 10.
- 11.
- 12. Gait in parkinsonism:phenomenology PD: stooped posture, flexed adducted arms, and loss of arm swing. Reduced arm swing during gait is often the first presenting feature of PD. Decreased height and length of step with a shuffling gait . MSA: Gait affected throughout the disease course , may be parkinson or cerebellar type. PSP: classic phenotype ambulate with an erect posture and abducted arms .en bloc turning (minimal trunk rotation while turning around). VP: characterized by start- and turn hesitation, short steps, a widened base, and imbalance with an inappropriate postural response may resemble the abnormal gait of NPH
- 13. POSTURAL ABNORMALITIES FLEXED POSTURE CAMPTOCORMIA STRIATAL HAND ANDTOE PD ANTECOLLIS MSA ERECT POSTURE PSP WITH DYSTONIC POSTURING WILSON DISEASE LATERAL DEVIATION PISA SIGN MSA WITH DYSTONIC POSTURING CBD
- 14. FACIES HYPOMIMIA. REDUCED BLINK RATE,DROOLING SALIVA PD DIP ATYPICAL SPONTANEOUS OR LEVODOPA-INDUCED DYSTONIA OR DYSKINESIA, WHICH MAINLY AFFECTS THE OROFACIAL MUSCLES MSA SEVERLY REDUCED BLINK RATE, PROCERUS SIGN, MONA LISA FIXITY OF GAZE, PSP
- 15. SPEECH HYPOKINETIC DYSARTHIA HYPOPHONIC, MONOTONOUS PD quivery, croaky, strained, high- pitchedspeech MSA slurred, lower pitched, growling quality of speech PSP MIXED DYSARTHIA hypophonic and spastic CBD
- 16. OCULOMOTAR ABNORMALITIES IMPAIRMENT IN VERTICALSACCADIC MOVEMENT. IMPAIRED DOWNWARD OPTICOKINETIC NYSTAGMUS . SQUARE WAVE JERKS, CONVERGENCE INSUFFICIENCY, REDUCED BLINK RATE, EYELID OPENING APRAXIA AND BLEPHAROSPASM. PSP SQUARE WAVE JERKS , OCULAR DYSMETRIA , WITH NORMAL VELOCITY AND LATENCY, AS WELL AS NYSTAGMUS MSA NYSTAGMUS, CONJUGATE OCULAR PALSY, SACCADIC ALTERATIONS, AND OCULOGYRIC CRISES . THE KAYSER–FLEISCHER RING WILSON DISEASE
- 17. Non-motor manifestation HYPOSMIA Maybe earliest sign in PD. Absent in others. RBD MSA>PD Autonomic dysfunction Early then MSA Constipation PD, MSA Dermatitis, eczema PD Sensory abnormalities (Pain, paresthesia, RLS) PD Cortical sensory loss-CBD Mantri S , Morley JF , Siderowf AD. The importance of preclinical diagnostics in Parkinson disease. Parkinsonism Relat Disord 2019;64:20–8
- 18. Cognitive and behavioraldisorders Anxiety and depression PD Changes in insight, disinhibition and apathy PSP Profound cognitive difficulties PSP, CBD Executive dysfunction PSP,MSA Early cognitive decline DLB Fluctuating cognition and attention, visual hallucination DLB Mantri S , Morley JF , Siderowf AD. The importance of preclinical diagnostics in Parkinson disease. Parkinsonism Relat Disord 2019;64:20–8
- 20. HISTORY • Response tomedications: Absence of benefit from adequate dosages of dopaminergic drugs, suggests a diagnosis of secondary causes of parkinsonism or one of the Parkinson- plus syndromes. • In IPD, psychiatric and autonomic side effects from dopaminergic drugs are not uncommon but usually appear when the illness is at least moderately advanced. • If dopaminergic drugs produced psychiatric side effects in early illness such as hallucinations or autonomic symptoms then it suggest the possibility of DLB, and the latter indicate MSA.
- 21. HISTORY • Medication usage.Patients must be asked if they are currently taking or have recently received antidopaminergic drugs such as neuroleptics, reserpine, or metoclopramide. • Toxic exposure. Exposure to toxins such as manganese or carbon monoxide must be ascertained because both can result in parkinsonism. Less common causes include mercury, carbon disulfide, methanol, and cyanide.
- 22. • Family history.Patients with Mendelian pattern of inheritance constitute a small minority of the overall Parkinson’s disease (PD) population. • Heritable disorders that can mimic PD include Wilson’s disease (autosomal recessive [AR]), juvenile Huntington’s disease (HD; autosomal dominant [AD]), and essential tremor (ET; AD with variable penetrance).
- 23. MDS-Unified Parkinson DiseaseRating Scale (MDS-UPDRS) Parkinsonism — Motor parkinsonism is an essential criterion of PD and requires both of the following : • Bradykinesia • Rest tremor or rigidity Supportive criteria — Supportive criteria are features that increase confidence in the diagnosis of PD : • A clear benefit from treatment with dopaminergic drugs, especially if the response is dramatic. (Note that tremor may not respond to levodopa in some patients, though bradykinesia and rigidity should improve.) In the absence of clear documentation of initial response, a dramatic response can be classified as one of the following: Unequivocal and marked on-off fluctuations, which must have at some point included predictable end-of-dose wearing off. • The presence of levodopa-induced dyskinesia. • Rest tremor of a limb (usually unilateral at onset), documented on previous or current clinical examination. • The presence of either olfactory loss or cardiac sympathetic denervation on metaiodobenzylguanidine (MIBG, iobenguane I-123) scintigraphy.
- 24. Red flags —Red flags are potential signs of alternate pathology, though with a low or uncertain specificity: 1. Rapid progression of gait impairment requiring the regular use of a wheelchair within five years of onset. 2. A complete absence of progression of motor symptoms or signs over five or more years unless stability is related to treatment. 3. Early bulbar dysfunction: severe dysphonia or dysarthria or severe dysphagia within the first five years. 4. Inspiratory respiratory dysfunction: either diurnal or nocturnal inspiratory stridor or frequent inspiratory sighs. 5. Severe autonomic failure in the first five years of disease. 6. Recurrent (more than once a year) falls because of impaired balance within three years of onset. 7. Disproportionate anterocollis (involuntary flexion of the neck) or contractures of hand or feet within the first 10 years. 8. Absence of any of the common nonmotor features of PD despite five years disease duration. 9. Otherwise-unexplained pyramidal tract signs, defined as pyramidal weakness or clear pathologic hyperreflexia (excluding mild reflex asymmetry and isolated extensor plantar response). 10. Bilateral symmetric parkinsonism. The patient or caregiver reports bilateral symptom onset with no side predominance, and no side predominance is observed on objective examination.
- 25. Absolute exclusion criteria 1.Unequivocal cerebellar abnormalities, such as cerebellar gait, limb ataxia, or cerebellar oculomotor abnormalities. 2. Downward vertical supranuclear gaze palsy, or selective slowing of downward vertical saccades. 3. Diagnosis of probable behavioral variant frontotemporal dementia or primary progressive aphasia within the first five years of disease. 4. Parkinsonian features restricted to the lower limbs for more than three years. 5. Treatment (currently or within the past year) with a dopamine receptor blocker or a dopamine-depleting agent in a dose and time course consistent with drug-induced parkinsonism. 6. Absence of observable response to high-dose levodopa despite at least moderate severity of disease. 7. Unequivocal cortical sensory loss, clear limb ideomotor apraxia, or progressive aphasia. 8. Normal functional neuroimaging of the presynaptic dopaminergic system.
- 26. PSP Basic features forthe diagnosis of PSP of any phenotype and at any stage include mandatory inclusion criteria, mandatory exclusion criteria, and context-dependent exclusion criteria . Mandatory inclusion criteria: • Sporadic occurrence • Age 40 years or older at onset of first PSP-related symptom • Consider any new-onset neurologic, cognitive, or behavioral deficit that subsequently progresses during the clinical course in absence of other identifiable cause as a PSP-related symptom.
- 27. Mandatory clinical exclusioncriteria: 1. Predominant, otherwise unexplained impairment of episodic memory, suggestive of Alzheimer disease. 2. Predominant, otherwise unexplained autonomic failure (eg, orthostatic hypotension suggestive of multiple system atrophy or Lewy body disease. 3. Predominant, otherwise unexplained visual hallucinations or fluctuations in alertness, suggestive of dementia with Lewy bodies. 4. Predominant, otherwise unexplained multisegmental upper and lower motor neuron signs, suggestive of motor neuron disease (pure upper motor neuron signs are not an exclusion criterion). 5. Sudden onset or step-wise or rapid progression of symptoms, in conjunction with corresponding imaging or laboratory findings, suggestive of vascular etiology, autoimmune encephalitis, metabolic encephalopathies, or prion disease. 6. History of encephalitis. 7. Prominent appendicular ataxia. 8. Identifiable cause of postural instability (eg, primary sensory deficit, vestibular dysfunction, severe spasticity, or lower motor neuron syndrome).
- 28. Mandatory imaging exclusioncriteria: • Severe cerebral leukoencephalopathy • Relevant structural abnormality (eg, normal pressure or obstructive hydrocephalus; basal ganglia, diencephalic, mesencephalic, pontine or medullary infarctions, hemorrhages, hypoxic-ischemic lesions, tumors, or malformations) Context-dependent imaging exclusion criteria: • In syndromes with sudden onset or step-wise progression, exclude stroke, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) or severe cerebral amyloid angiopathy, evidenced by diffusion-weighted imaging (DWI), fluid attenuated inversion recovery, or T2* MRI • In cases with very rapid progression, exclude cortical and subcortical hyperintensities on DWI-MRI suggestive of prion disease
- 29. Context-dependent laboratory exclusioncriteria: In patients with PSP-CBS, exclude primary Alzheimer disease pathology (typical cerebrospinal fluid constellation [ie, both elevated total tau and phospho-tau protein and reduced beta-amyloid 42] or pathological beta-amyloid PET imaging) In patients <45 years of age, exclude: • Wilson disease • Niemann-Pick disease, type C • Hypoparathyroidism • Neuroacanthocytosis • Neurosyphilis In rapidly progressive patients, exclude: • Prion disease • Paraneoplastic encephalitis (anti-ma2, iglon-5) In patients with suggestive features (ie, gastrointestinal symptoms, arthralgias, fever, younger age, and atypical neurologic features such as myorhythmia), exclude Whipple disease
- 38. LABORATORY TEST CBC/PBF HEMOLYTIC ANAEMIAWD ACANTHOCYTES NEUROACANTHOCYTOSIS BLOOD CHEMISTRY ABNORMAL LFT WD HYPOCALCEMIA LOW PARATHORMONE HYPOPARATHYROIDSM ELEVATED CREATINE KINASE NEUROACANTHOCYTOSIS ELEVATED LACTATE AND LACTIC ACIDOSIS MITOCHONDRIAL CYTOPATHIES
- 39. INVESTIGATIONS 1. Plain X-rays.Spine X-rays may reveal ankylosing spondylitis or osteoarthritis as the cause of mechanical limitation of movement. 2. CT or MRI of the brain. CT may demonstrate a neoplasm, stroke, hydrocephalus, basal ganglia calcification, atrophy, or sequelae of trauma. 3. MRI of the brain is more desirable. Several characteristic MRI patterns that are suggestive of specific hypokinetic disorders are listed below: a. Many lacunar strokes. vascular parkinsonism b. Large ventricles, out of proportion to cerebral atrophy; transependymal flow: NPH c. Caudate atrophy. HD d. Decreased T2 signal in striatum. MSA e. Homogeneous decreased T2 signal or decreased T2 signal with a central hyperintensity (Tiger’s eye) in the globus pallidus: NBIA f. Striatal necrosis. Wilson’s disease, Leigh’s disease, and CO intoxication g. Midbrain atrophy. PSP h. Asymmetric frontoparietal atrophy. CBGD
- 40. INVESTIGATIONS PET or SPECT.With modern analysis techniques, fluorodeoxyglucose PET, by characterizing the regional cerebral metabolism pattern, can distinguish PD, MSA, and PSP from one another with >90% accuracy. • In IPD, either of these two modalities demonstrates a loss of dopaminergic nigral cells. • The major clinical usefulness of Ioflupane SPECT is that it is very accurate in distinguishing IPD from mimicking conditions that do not involve dopamine-producing cells such as ET, dystonic tremor, or drug-induced parkinsonism.
- 41. INVESTIGATIONS 1. ECG. Heartblock may be present in mitochondrial cytopathy. 2. EEG. Epileptic activity or focal slowing may appear with focal lesions (stroke and tumor). Slow background activity is seen in some primary dementias. Periodic triphasic complexes may be present in CJD . 3. EMG/nerve conduction studies. Mild nerve conduction slowing suggestive of axonal polyneuropathy is seen in neuroacanthocytosis. Myopathic findings on EMG may be present in cases of mitochondrial cytopathies.
- 42. INVESTIGATIONS CSF analysis. Elevatedprotein and pleocytosis can be detected in CNS infections. The presence of high levels of the 14-3-3 protein in CSF is highly suggestive of CJD. Special diagnostic tests. 1. Wilson’s disease. Low ceruloplasmin, low serum copper, increased 24-hour urinary copper excretion, and Kayser– Fleischer ring on slit lamp examination of the cornea are all suggestive of Wilson’s disease. 2. NPH- Tap test.
- 43. INVESTIGATIONS Genetic testing. MonogenicPD is found in approximately 3% of IPD patients and mutations in these PD genes are most common in those with an early age of onset or those belonging to certain ethnic groups. • In patients with onset before age 51, almost 20% have a mutation in one of these genes, most commonly parkin, followed by LRRK2. • In individuals developing PD under the age of 20, as many as 77% have a mutation of the Parkin gene. Common AD PD subtypes include PARK1 (SCNA missense mutation), PARK4 (SCNA duplications/triplications), and PARK8 (LRRK2 mutation). • Common AR PD syndromes are PARK2 (parkin), PARK6 (PINK1), and PARK7 (DJ-1).
- 44. Normal Visualization ofdopamine transporters at 123I ioflupane SPECT and FDG PET IPD
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- 51. TAKE HOME MESSAGE •Careful history taking is essential. • Past medical and psychiatric history, family history, and occupational or environmental exposure to toxins will reveal most causes of secondary parkinsonism. • Disease onset at a young age, a strong family history, lack of resting tremor, absent response to levodopa and early appearance of postural instability, gait disorder, dysautonomia, aphasia, apraxia, supranuclear gaze palsy, cortical sensory loss, alien limb phenomenon, pyramidal signs or dementia should be considered red flags in the history suggesting a diagnosis other than IPD. • General physical examination is important because it may reveal signs of a systemic disease that is contributing to secondary parkinsonism.
- 52. REFERENCES 1. Bradley's Neurologyin Clinical Practice.2021.8th ed. 2. Goldman SM, Tanner C. Etiology of Parkinson's's disease. In: Jankovic J, Tolosa E, editors. Parkinson's's disease and movement disorders, 6rd ed. Baltimore, MD: Lippincott-Williams and Wilkins; 2017. p. 133-58 3. Marsden’s book of movemeny disorder.2016 4. Saeed, U., Compagnone, J., Aviv, R.I. et al. Imaging biomarkers in Parkinson’s disease and Parkinsonian syndromes: current and emerging concepts. Transl Neurodegener 8 (2017). 5. Obeso JA , Stamelou M , Goetz CG , et al Past, present, and future of Parkinson's disease: a special essay on the 200th anniversary of the shaking palsy. Mov Disord 2017;:1264–310 6. Armstrong MJ , Okun MS . Diagnosis and treatment of Parkinson disease. JAMA 2020;323:548–60 7. Mantri S , Morley JF , Siderowf AD. The importance of preclinical diagnostics in Parkinson disease. Parkinsonism Relat Disord 2019;64:20–8 8. Kalia LV . Diagnostic biomarkers for Parkinson's disease: focus on α-synuclein in cerebrospinal fluid. Parkinsonism Relat Disord 2019;:21–5 9. Niemann N , Jankovic J . Juvenile parkinsonism: differential diagnosis, genetics, and treatment. Parkinsonism Relat Disord 2019;67:74–89 10. Mehanna R , Jankovic J . Young-Onset Parkinson's disease: its unique features and their impact on quality of life. Parkinsonism Relat Disord 2019;65:39–48
- 53.
- 67. Features Suggestive ofAtypical PD
- 68. LABORATORY STUDIES • IPD.In classical IPD where the diagnosis is strongly suggested by the history and physical examination, neuroimaging is not necessary. • IPD is commonly asymmetric, but if symptoms or signs of parkinsonism are remarkably asymmetric resulting in severe involvement on one side , MRI is indicated to evaluate for the possibility of unilateral structural basal ganglia pathology.
- 69. • CT ofthe brain are usually unremarkable in IPD. • MRI s/o absent swallow tail” sign. • A positron-emission tomography (PET) scan shows decreased fluorodopa uptake in the striatum but no striatal abnormality in fluorodeoxyglucose scans.
- 70. • SPECT canbe used to differentiate diseases with striatal dopaminergic degeneration, namely, IPD and PD-plus syndromes, from ET, drug-induced parkinsonism, dystonic tremor, psychogenic parkinsonism, and vascular parkinsonism without striatal dopaminergic degeneration. • Transcranial sonography (TCS) is a cost-effective, widely available technique to visualize cerebral echogenic changes with high spatial resolution. The finding of substantia nigra heterogeneity (>20 mm) through the preauricular window is 90% specific for IPD.
- 71. CLINICAL FEATURES TAUPATHYSYNUCLEOPATHY Age of onset 7th 6th Initial symptoms Postural &gait disorder Tremor & bradykinesia Family history - +/- Multi infarct state +/- - Dementia +/- +/- Downgaze ophthalmoparesis + - Eyelid abnormalities + +/- Pseudobulbar palsy + +/- Gait Wide,stiff,unsteady Slow shuffling,narrow,festinating Rigidity Axial(neck) Generalised
- 72. Corticobulbar signs +/-- Symmetry of findings + - Weight loss - + Improvement with DA drugs _ + Levodopa induced dyskinesias _ +
- 73. PD: hypokinetic dysarthria.Patients develop a soft voice with accompanying slurring MSA: hypokinetic speech, patients may develop ataxic and, more rarely, spastic qualities in the voice, resulting in quivery, croaky, strained, high- pitched speech PSP: hypokinetic dysarthria, which is commonly associated with spastic elements, causing a slurred, lower pitched, growling quality of speech. CBD: dysarthria of a mixed character (hypophonic and spastic). Later stages of CBD, the peculiar characteristics of apraxic speech (slow speaking rate, SPEECH Armstrong MJ , Okun MS . Diagnosis and treatment of Parkinson disease. JAMA 2020;323:548–60
- 74. Akinesia/Bradykinesia in parkinsonism: phenomenology PD:almost always asymmetrical MSA: more often asymmetrical than symmetrical, but always bilateral PSP: marked axial, minimal appendicular (in classical Richardson’s syndrome) CBD: severe and markedly asymmetrical Vascular: in the classical “lower body” form predominantly affecting lower limbs, stepwise progression Armstrong MJ , Okun MS . Diagnosis and treatment of Parkinson disease. JAMA 2020;323:548–60
- 75. Tremor in parkinsonism:phenomenology PD: unilateral or asymmetric pill-rolling rest tremor. A postural/kinetic component (re-emergent tremor) may also be present MSA: postural/kinetic tremor frequent (~2/3 of the cases). Often incorporating myoclonus, that gives it an irregular quality (“jerky postural tremor”) PSP: uncommon, only in the PSP-P phenotype CBD: the common myoclonic jerks of the involved limb(s) can clinically resemble tremor DIP: onset is abrupt, both resting and postural tremor, arms>leg, symmetrical. Subside after ofending drug removed. Armstrong MJ , Okun MS . Diagnosis and treatment of Parkinson disease. JAMA 2020;323:548–60
- 76. IMAGING Posterior putaminal atrophywith marginal hyperintensity on T2. Pontine atrophy with cross like hperintensity, MCP atrophy and atrophy of superior vermis. FDG PET demonstrate hypometabolism of putamen and cerebellum MSA Atophy of midbrain and superior cerebellar peduncle and dilation of third ventricle. Mid-sagittal plane s/o hummingbird sign and axial images s/o morning glory sign. FDG PET images show hypometabolism in the posterior frontal lobes and basal ganglia, worse on the right side . PSP Asymmetric frontoparietal atrophy. Hyperintensity in the subcortical white matter in the rolandic region on FLAIR images with asymmetric atrophy in the cerebral peduncle, and atrophy in the midbrain tegmentuM PET scans show reduced [18F]fluorodopa uptake in the caudate and putamen and markedly asymmetrical cortical hypometabolism, especially in the superior temporal and inferior parietal lobe CBD h typical PD is usually normal; but a high-field-strength (1.5 T) heavily T2-weighted MRI may show a wider area of lucency in the SN FDG PET image shows parietal and strital hypometabolism IPD