30/7/2014 PubMed Central, Figure 6: Ann N Y Acad Sci. Jan 2010; 1184: 1554. doi: 10.1111/j.1749-6632.2009.05115.x

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902006/figure/F6/ 1/2

Figure 6

Schematic representation of the brain, spinal cord, and key peripheraland autonomic structures which can be affected by Lewy bodydisease pathology, and the clinical features associated withdysfunction of each structure. The structures (abbreviations) andlikely associated clinical features are as follows: olfactory bulb(OB)=anosmia, tuberomamillary nucleus (TMN)=alteredarousal/sleep, lateral hypothalamus (LHT)=hypersomnia, nucleusbasalis of Meynert (NBM)=cognitive impairment, hippocampalformation (HF)=cognitive impairment, neocortex (N)=cognitive

http://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=2902006_nihms198346f6.jpg

30/7/2014 PubMed Central, Figure 6: Ann N Y Acad Sci. Jan 2010; 1184: 1554. doi: 10.1111/j.1749-6632.2009.05115.x

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902006/figure/F6/ 2/2

impairment, substantia nigra (SN)=parkinsonism, pedunculopontinenucleus (PPN)=altered arousal/attention, raphe nucleus(RN)=depression, locus ceruleus (LC)=depression, sublaterodorsalnucleus (SLD)=? RBD, magnocellular reticular formation (MCRF)=?RBD, intermediolateral cell column (ILDN)=orthostatism,sympathetic innervation of the heart (H)=cardiac dysfunction, entericinnervation of the intenstines (I)=constipation, and autonomicinnervation of the sex organs (SO)=impotence

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Editor : Dr. Siddharth N. Shah

NOVEMBER 2012 VOL. 60

Pictorial CME

Hummingbird Sign, Penguin Sign and Mickey Mouse Sign in Progressive Supranuclear Palsy

Shobha M Itolikar*, Santosh B Salagre**, Chetan R Kalal***

*Assistant Professor, **Associate Professor, ***Postgraduate Student, Department of Medicine, Seth G.S. Medical College and K.E.M. Hospital, Parel Mumbai-400012.

Received: 15.01.2011; Revised: 15.04.2011; Accepted: 07.06.2011

A fifty year old male was brought by his wife with insidious onset forgetfulness, slurring of speech, slowness of movements and frequent falls. There was no history of

vomiting, seizures, limb weakness, diplopia, dysarthria, dysphagia, nasal regurgitation or facial asymmetry. Examination findings were remarkable for borderline

impairment of memory (MMSE score= 27 / 30), slurred speech, conjugate vertical gaze palsy, slowness of horizontal saccades and bradykinesia. Glabellar tap was

positive. His blink rate was 6-8/min. Cogwheel rigidity, tremors or autonomic features were not present in this patient.MRI Brain revealed flattening of superior profile of

midbrain due to midbrain tegmental atrophy with widening of interpedencular cistern giving the impression of a hummingbird and Mickey mouse appearance of the

brainstem (Figures 1 and 2).Based on the clinical and radiographic features , he was diagnosed as a case of

Progressive Supranuclear Palsy ( Steele-Richardson-Olszewski syndrome). Progressive supranuclear palsy (PSP) is a form of Parkinsonism which is a

neurodegenerative disorder. Along with diseases like multisystem atrophy, corticobasal degeneration, dementia with Lewy bodies and frontotemporal dementia, it

constitutes the Parkinson-plus syndromes. The ensuing Table 1 compares this disorder with idiopathic Parkinson disease

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The above signs describing the imaging findings in the form of animate silhouettes are just a few of the entire gamut of neurological menagerie (erstwhile zoos) that

exist in medical parlance3 which make for easy remembrance of disease features for the clinician.

References

1. Harrisons Principles of Internal Medicine, 17th Edition. Fauci, Braunwald, Kasper; Vol. II, Chapter 366.

2. Stacy M, Jankovic J. Differential diagnosis of Parkinsons disease and the parkinsonism plus syndromes. Neurol Clin 1992;10:341-59.

3. JM Schott. A neurological MRI menagerie. Pract Neurol 2007;7:186-90.

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Neuromuscular disease Acquired peripheral demyelinating neuropathy Hereditary peripheral

demyelinating neuropathy

Anterior horn cell disease

Acute Inflammatory Demyelinating Poly- radicucloneuropathy (GBS)

Chronic Inflammatory Demyelinating Poly- radiculoneuropathy (CIDP)

Multifocal acquired Demyelinating sensory and motor Neuropathy (MADSAM), with Persistent Conduction Block (Lewis-Sumner syndrome)

Multifocal Motor Neuropathy (MMN)

Hereditary Sensorimotor Neuropathy (HSMN Charcot-Marie-Tooth disease CMT typ 1 AD

Amyotrophic Lateral Sclerosis

Age of onset all ages all ages 23-72 yrs 15-70 yrs 1st 2nd decade 40-70 yrs Weakness symmetric symmetric Asymmetric asymmetric Symmetrical asymmetric Motor > sensory Motor > sensory Motor > sensory Distribution Distal-Proximal Distal-Proximal Distal>Proximal Distal>Proximal

extremity Distal Distal>Proximal

extremity, bulbar Lower>Upper Extremity Lower>Upper Extremity Upper>Lower Extremity Upper>Lower Upper-lower

extremity Upper-Lower

Progression acute insidious/stepwise progressive or relapsing neuropathy,

Insidious/ stepwise

stepwise/ insidious

Slowly progressive rapid

An acute infectious illness precedes weakness in two thirds

An antecedent infectious illness is uncommon

Fascicul./Cramps

rare rare Rare common very common

Deep tendon reflexes

reduced/absent reduced/absent Reduced/absent reduced/normal Absent increased

Sensory loss present present Present absent/minor Present absent SNAP absent/reduced absent/reduced absent/reduced normal/reduced Reduced or absent normal CMAP reduced reduced Reduced reduced/normal Reduced or absent reduced Conduction block

present present Present present Absent absent

MCV slowed slowed slowed/normal slowed/normal Slow normal CSF protein increased often increased often increased normal Mildly high normal GM1 Antibodies

+/ +/ +/ 22-84% ; mean 50% +/

Myelinated fibers show segmental demyelination during the first few days. Segmental remyelination occurs subsequently.

segmental demyelination and remyelination, onion bulbs, fibrosis and little or no lymphocytic infiltration of tissue.

Sural nerve biopsy

abnormal Abnormal Abnormal minor abnormalities normal

Differential diagnostic features of acquired demyelinating neuropathies. SNAP = sensory nerve action potential, CMAP = compound muscle action potential, MCV = motor conduction velocity NOTE Acquired, or non-hereditary, chronic demyelinating neuropathies, with the exception of certain drug toxicities as may be seen with Amiodarone, are considered to be autoimmune, and classified under - the general heading of chronic inflammatory demyelinating polyneuropathy (CIDP). The typical presentation is that of proximal and distal weakness with distal large fiber sensory

loss, - but approximately 50% of patients have atypical presentations, probably reflecting the distribution of lesions. These include o Multifocal Motor Neuropathy (MMN), o Multifocal Acquired Demyelinating Sensory and Motor (MADSAM) neuropathy, A similar disorder of sensory ataxia MADSAM due to inflammation confined to the dorsal roots known as chronic immune sensory polyradiculopathy or CISP may be a restricted form of CIDP Normal nerve conduction studies, characteristic somatosensory evoked potential (SSEP) abnormality, enlarged nerve roots, elevated CSF protein, and inflammatory

hypertrophic changes of sensory nerve rootlet tissue, we suggest the term chronic immune sensory polyradiculopathy (CISP) for this syndrome. This condition preferentially affects large myelinated fibers of the posterior roots, may respond favorably to treatment.

o Distal Acquired Demyelinating Predominantly Sensory (DADS) Neuropathy, o and Sensory CIDP

- If the lesions are demyelinating, as in MMN or MADSAM, then the neuropathies are presumed to be autoimmune. In the case of axonal neuropathies, however, the presence of multifocality may be the only distinguishing feature b/w autoimmune-axonal and non autoimmune-axonal neuropathy. - Such multifocal axonal neuropathies include o nonsystemic vasculitic neuropathy, o multifocal axonal sensory and motor neuropathy (MASAM) o and multifocal sensory neuropathy or sensory ganglioneuritis

- If other causes for multifocal sensory neuropathy, such as Lyme disease or diabetes are excluded, then immune mechanisms should be considered.

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Ahmed Ismael Rwandizy shared a photo to the group %E2%80%8EMRCP part1, 2 written and PACES

.E2%80%8E%

15 hrs

Ahmed Ismael Rwandizy %E2%80%8Einternist clubTreatment of acute haemorrhagic stroke ???

1. Cannula

3. NPO

2.NG tube

3. Foley's catheter

4.Semi-setting position

5. Paracetamol ampoule

6. Decadrone ampoule

7. Mannitol 20% 200 cc within 20 minutes

8. Plasil ampoule

9. Oxygen if Spo2 less than 94 (less than 88 in case of chronic pulmonary compromise)

10. Assess regularly for intubation

11. Control blood sugar (both low and high levels require interventions)

12. Control Bp (Bp: Systolic > 23 mmHg and diastolic > 130 mmHg reqiure control to prevent expansion of haemorrhage; use short acting

agents and the aim is to decrease Bp by 20% in first 1-4 hours, re-measure blood pressure every 30 minutes within this period then hourly

and 2-hourly and so.) Labetalol and Nicardipine are preferable agents

Remember keep an eye on the Spo2 and be ready for advanced life support at any moment ...

Lastly pray for your patient..

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Facies special : %E2%80%AA#%E2%80%8EHighYield%E2%80%AC

1. Mask like facies = parkinsonism.2. Elfin facies = william's syndrome.3. Moon facies = cushing's syndrome.4. Snarling facies = myasthenia gravis.5. Mitral facies = mitral stenosis.6. Ashen grey facies = myocardial infarction.7. Mouse facies = chronic renal failure (crf)8. Adenoid facies = adenoid hypertrophy.9. Leonine facies = lepromatous leprosy .10. Bird facies = pierre robin syndrome.11. Mongoloid facies = down's syndrome.12. Coarse facies = most of the inborn errors of metabolism (iem) viz. The muco- polysaccharidoses (mps), mucolipidoses(ml), fucosidoses mannosidoses, sialidoses, aspartylglycosaminuria, generalised gangliosidosis(gml ) and austin'svariant of metachromatic leukodystrophy due to multiple sulfatase deficiency (mld-msd) have similar appearing facies.13. Syphilitic facies = congenital syphilis ( bull dog jaw)14. Hippocratic face = (also known as"hippocratic facies"; eyes are sunken, temples collapsed, nose is pinched with crustson the lips and the forehead is clammy).15. Potter facies = oligohydramnios16. Amiodarone facies = (deep blue discoloration around malar area and nose)17. Acromegalic facies = acromegaly18. Marfanoid facies = marfan's syndro19. Mesnarling facies = myasthenia gravis20. Myotonic facies = myotonic dystrophy21. Torpid facies = myxoedema22. Mouse facies = chronic renal failures23. Myxoedemamouse facies = chronic renal failure24. Plethoric facies = cushing's syndrome and polycythemia vera25. Ashen grey facies = myocardial infarction26. Gargoyle facies = hurler's syndrome27. Monkey facies = marasmus28. Hatchet facies = myotonica atropathica29. Guerilla like face = acromegaly30. Bovine facies or cow face = cranio fascial dysostosis or crouzons syndrome31. Marshall halls facies = hydrocephalus32. Frog face = intra nasal disease33. Bird facies = (Pierre Robin Malformation)34. Chipmunk facies = ( Untreated Thalassemia major, Bullimia nervosa, Parotid sweling.35. Leonine facies = (Lepromatous Leprosy)36. Adenoid facies = (Adenoid hypertrophy)37. Torpid or Myxedematous facies = (Myxedema)38. Mask like or Parkinsonian facies = (Parkinsonism)39. Acromegalic facies = (Acromegaly)40. Cushingoid facies = (Cushing syndrome)41. Gargoyle facies = (Hurler syndrome)

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