Difference between revisions of "Neuromuscular pathology"

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Muscle pathology is dealt together with neurologic disease as, at the presentation, they are not infrequently impossible to definitely distinguish.
Muscle pathology is dealt together with neurologic disease as, at the presentation, they are not infrequently impossible to definitely distinguish.


==Work-up==
=Work-up=
===General===
===General===
#Clinical history, including family history.
#Clinical history, including family history.
Line 180: Line 180:
#Myopathy - something is wrong with the muscle fibres.
#Myopathy - something is wrong with the muscle fibres.


==Stains for muscle biopsies==
=Stains for muscle biopsies=
===Standard===
===Standard===
{| class="wikitable"
{| class="wikitable"
Line 292: Line 292:
***Same protein that that in implicated in [[ALS]] and [[frontotemporal dementia]].
***Same protein that that in implicated in [[ALS]] and [[frontotemporal dementia]].


==Inflammatory myopathy==
=Inflammatory myopathy=
DDx:
DDx:
#Polymyositis.
#Polymyositis.
Line 334: Line 334:
*Periodic paralysis.
*Periodic paralysis.


=Specific entities=
==Amyotrophic lateral sclerosis==
==Amyotrophic lateral sclerosis==
===General===
===General===
Line 435: Line 436:
*A type of congenital myopathy.
*A type of congenital myopathy.
*Paediatric thingy.
*Paediatric thingy.
==Drug-induced rhabdomyolysis==
*AKA ''drug-induced acute necrotizing myopathy''.
===General===
Clinical:<ref name=pmid15021204>{{Cite journal  | last1 = Coco | first1 = TJ. | last2 = Klasner | first2 = AE. | title = Drug-induced rhabdomyolysis. | journal = Curr Opin Pediatr | volume = 16 | issue = 2 | pages = 206-10 | month = Apr | year = 2004 | doi =  | PMID = 15021204 }}</ref>
*Myalgias.
*Myoglobinuria.
*Increased elevated serum creatine kinase (CK).
Causes:
*Ecstasy (MDMA).
*Statins.
===Microscopic===
Features:
*Muscle [[necrosis]].
**Fibre collapse = increased staining on [[H&E stain|H&E]], [[HPS stain|HPS]].
**Karyolysis - loss of nuclei.
**Macrophage (phagocytosis) clean-up = pale moth-eaten appearance (seen well on [[PAS stain|PAS]]).
*No inflammation.
*No perifascicular atrophy.
Images:
*[http://path.upmc.edu/cases/case184/micro.html Drug-induced rhabdomyolysis - several images (upmc.edu)].
===Stains===
*PAS +ve fibres (macrophages).
===IHC===
*CD45 -ve (no lymphocytes).
===EM===
*Negative for [[tubuloreticular inclusions]].


==Limb-girdle muscular dystrophy==
==Limb-girdle muscular dystrophy==
Line 458: Line 492:
*Inflammatory myopathies.
*Inflammatory myopathies.


=Groups of disorders=
==Mitochondrial disorders==
==Mitochondrial disorders==
===General===
===General===
Line 495: Line 530:
*[http://commons.wikimedia.org/wiki/File:Denervation_atrophy_-_atp94_-_high_mag.jpg Type 2 fibre atrophy - ATPase pH 9.4 - high mag. (WC)].
*[http://commons.wikimedia.org/wiki/File:Denervation_atrophy_-_atp94_-_high_mag.jpg Type 2 fibre atrophy - ATPase pH 9.4 - high mag. (WC)].


==Drug-induced rhabdomyolysis==
=Nerve stuff=
*AKA ''drug-induced acute necrotizing myopathy''.
===General===
Clinical:<ref name=pmid15021204>{{Cite journal  | last1 = Coco | first1 = TJ. | last2 = Klasner | first2 = AE. | title = Drug-induced rhabdomyolysis. | journal = Curr Opin Pediatr | volume = 16 | issue = 2 | pages = 206-10 | month = Apr | year = 2004 | doi =  | PMID = 15021204 }}</ref>
*Myalgias.
*Myoglobinuria.
*Increased elevated serum creatine kinase (CK).
 
Causes:
*Ecstasy (MDMA).
*Statins.
 
===Microscopic===
Features:
*Muscle [[necrosis]].
**Fibre collapse = increased staining on [[H&E stain|H&E]], [[HPS stain|HPS]].
**Karyolysis - loss of nuclei.
**Macrophage (phagocytosis) clean-up = pale moth-eaten appearance (seen well on [[PAS stain|PAS]]).
*No inflammation.
*No perifascicular atrophy.
 
Images:
*[http://path.upmc.edu/cases/case184/micro.html Drug-induced rhabdomyolysis - several images (upmc.edu)].
 
===Stains===
*PAS +ve fibres (macrophages).
 
===IHC===
*CD45 -ve (no lymphocytes).
 
===EM===
*Negative for [[tubuloreticular inclusions]].
 
==Nerve stuff==
===General===
===General===
*Most common biopsy: sural nerve.
*Most common biopsy: sural nerve.
Line 559: Line 561:
*Toxic polyneuropathy (drug toxicity).<ref>URL: [http://path.upmc.edu/cases/case173.html http://path.upmc.edu/cases/case173.html]. Accessed on: 8 January 2012.</ref>
*Toxic polyneuropathy (drug toxicity).<ref>URL: [http://path.upmc.edu/cases/case173.html http://path.upmc.edu/cases/case173.html]. Accessed on: 8 January 2012.</ref>


==See also==
=See also=
*[[Neuropathology]].
*[[Neuropathology]].


==References==
=References=
{{reflist|2}}
{{reflist|2}}


==External links==
=External links=
*[http://moon.ouhsc.edu/kfung/jty1/NeuroHelp/ZNEWWU10.htm How to work up a muscle biopsy (ouhsc.edu)].
*[http://moon.ouhsc.edu/kfung/jty1/NeuroHelp/ZNEWWU10.htm How to work up a muscle biopsy (ouhsc.edu)].
*[http://neuromuscular.wustl.edu/lab/mbiopsy.htm Muscle biopsies (wustl.edu)].
*[http://neuromuscular.wustl.edu/lab/mbiopsy.htm Muscle biopsies (wustl.edu)].


[[Category:Neuropathology]]
[[Category:Neuropathology]]

Revision as of 01:52, 21 January 2012

Neuromuscular pathology is the study of muscle and neurologic disease associated with muscle dysfunction. It is a part of neuropathology.

Muscle pathology is dealt together with neurologic disease as, at the presentation, they are not infrequently impossible to definitely distinguish.

Work-up

General

  1. Clinical history, including family history.
  2. Laboratory studies, e.g. CK.
  3. Nerve conduction and electromyography studies.
  4. Muscle biopsy.

Clinical

  • Fasciculations - small involuntary muscle contraction, imply lower motor neuron lesion.
  • Reflexes - see physical examination.
  • Strength.

Laboratory studies

The CK suggest the type of disorder:[1]

  • High ~200-300X normal -- suggests myogenic.
  • Intermedidate ~20-30X normal -- possibly inflammatory.
  • Low ~2-5X normal -- possibly neurogenic.

Notes:

  • The CK value is most useful when it is very high.[2]
  • Normal CK values:[3]
    • Men: 24-195 unit/litre.
    • Women: 24-170 units/litre.

Muscle structure/histology

Macro to micro

Organization:[4]

  • Muscle - surrounded by epimysium.
    • Fascicle - surrounded by perimysium.
      • Muscle fibre - muscle cell.
        • Myofibrils - contractile elements within the muscle cell.

Notes:

  • This is similar for nerves:[5]
    • Nerve (surrounded by epineurium) -> Fascicle (surrounded by perineurium) -> Nerve fibre (surrounded by endoneurium).

Fibre types

 
 
 
Types
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Type 1
slow twitch
 
 
 
Type 2
fast twitch

List

Type 1 - AKA slow twitch:

  • Predominantly oxidative metabolism, i.e. have lots of mitochondria.

Type 2 - AKA fast twitch:

  • Predominantly glycolytic metabolism.

Mnemonic Slow red fat ox: Slow twitch fibres are (grossly) more red (due to mitochondria), lipid rich (fat) and primarily have oxidative metabolism.

Normal findings

Muscle-tendon junction

Features:

Muscle-nerve junction

Features:

  • Dunno. (???)

Images:

Muscle spindle

Features:

  • Weird looking muscle cell. (???)

Image: Muscle spindle (anhb.uwa.edu.au).[7]

Abnormal findings

Iatrogenic

  • Torn (muscle) fibres (in the process of extraction for examination):
    • Membrane intact.
    • Myofibril kaputt.
    • No inflammation.

Pathologic

Others:

Approach

General:

  1. Size variation - in groups (neurogenic) vs. singular (myogenic).
  2. Shape - angulated (neurogenic) vs. round (myogenic).
  3. Position of nuclei - peripheral (normal); central (myogenic; centronuclear myopathy[8]).
  4. Necrosis - suggests myogenic.
  5. Fibrosis - suggests myogenic.
  6. Inflammation - suggest myogenic vs. systemic inflammatory.

Other:

  1. Obvious abnormality vs. minimal change.
  2. Diffuse vs. focal change.

Processing of muscle biopsies

  1. Formalin fixed (formalin fixed-paraffin embedded).
  2. Frozen tissue for histology.
  3. Frozen tissue for biochemistry.
  4. Fragment for electron microscopy (glutaraldehyde fixed).

SMH labeling

  • "E" = "frozens"; done on frozen tissue.
    • IHC done on these.
    • May have the label "2" ... even though there is no part 2.
  • Blue slides = "plastics", i.e. plastic embedded.
    • Stained with methylene blue.[9] vs. toluidine blue. (???)
    • Thin sections: 0.1 - 1 micrometres.
  • Normal SMH numbering = "paraffin".

Patterns (pathologic)

Overview

 
 
 
 
 
 
 
 
Neuromuscular
pathology
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Neurogenic
 
 
Myogenic
 
 
Other/Mixed
Neurogenic Myogenic Notes Image
Shape of fibres angulated round round fibres[10]
Small fibres groups
("group atrophy") 		singular group atrophy[11]
Large fibres
 no +/-scattered "hypercontracted
fibres" 		DMD (WC)
Fibre type
grouping 		yes (d/t chronic
denervation +
reinnervation)[12] 		yes (???) based on ATPase,
NADH-TR stains 		ATPase 9.4[13], NADH-TR[14]

List

Neurogenic:

  • Angulated myocytes.
  • Groups of small fibres.
  • Apparent increase of nuclei.

Myogenic:

  • Round myocytes.
  • +/-Intense (darker) cytoplasm.
  • +/-Fibrosis (between fibres).
  • +/-Necrosis.

Detail

  1. Segmental demyelination - nerve/CNS abnormality.
  2. Axonal degeneration - nerve/CNS abnormality.
  3. Reinnervation - nerve injury.
  4. Myopathy - something is wrong with the muscle fibres.

Stains for muscle biopsies

Standard

Stain Comment Image
H&E stain routine H&E[15], H&E (WC)
Gomori trichrome good for nemaline rods,
mitochondrial pathology
(ragged red fibres - at edge
of myocyte) 		RRF (WC)
PAS glycogen storage disorders [1][16]
Congo red find amyloid; seen in
inclusion body myositis 		[2][17]
Oil red O lipid more in
type 1 fibres 		ORO
ATPase pH4.2
ATPase pH9.4 		should have "checkerboard
pattern" in normal; see table below 		[3][18]
NADH-TR should have "checkerboard
pattern" in normal;
type 1 fibres = light blue,
type 2 fibres = white

ATPase stain pattern/fibre type

Type 1
slow twitch 		Type 2
fast twitch
pH 4.2 dark light
pH 9.4 light dark

Special - mitochondrial pathology

Stain Comment Image
Succinate
dehydrogenase (SDH) 		stains mitochondria;
usu. +ve in mitochondrial disease[19] 		[4][20], SDH (WC)
Cytochrome oxidase (COX) stains mitochondria;
usu. -ve in mitochondrial disease 		[5][20]
COX-SDH used to look for mitochondrial disease

Enzymatic/genetic stuff

Stain Comment Image
Phosphorylase
Adenylate deaminase
Acid phosphatase (ACPH) necrosis (red)
Alkaline phosphatase (ALPH) regeneration (punctate - black)

Dunno:

IHC

  • Dystrophy panel.
    • Dystrophin[22] - Duchenne muscular dystrophy (onset usu. <3 years), Becker's muscular dystrophy (onset usu. 20s or 30s).
      • Membranous staining is normal. Loss of membranous staining = pathologic.
        • Tested with three antibodies -- as the protein is hueuge.
    • Spectrin - a cause of long QT syndrome. (???)
  • Lymphocytic markers (CD45, CD3, CD4, CD8, CD20).
  • MAC - inclusion body myositis.
  • APP - inclusion body myositis (?), axonal swellings.
  • Ubquitin - inclusion body myositis.
  • TDP-43 (also TDP43) - cytoplasmic staining in IBM.

Inflammatory myopathy

DDx:

  1. Polymyositis.
    • Disease of adults.
  2. Inclusion body myositis (IBM).
  3. Dermatomyositis.
    • May be associated with malignancy.

Partial invasion of muscle fibres

DDx:[23]

  • Polymyositis.
  • IBM.

Images:

DDx

Neurogenic:

  • Amyotrophic lateral sclerosis.
  • Spinal muscular atrophy.
  • Trauma.
  • Vascular disease.
  • Infective process.
  • ?Motor neuron disease.

Myopathic:

  • Inflammatory:
    1. Polymyositis.
    2. Inclusion body myositis.
    3. Dermatomyositis.
  • Duchenne muscular dystrophy.
  • Becker muscular dystrophy.
  • Limb-girdle muscular dystrophy.
  • Myotonic dystrophy.
  • Metabolic - glycogen storage disease.

Other:

  • Myasthenia gravis.
  • Mitochondrial myopathy.
  • Congenital fibre type disproportion.
  • Periodic paralysis.

Specific entities

Amyotrophic lateral sclerosis

General

  • Abbreviated ALS.
  • Affects - corticospinal tract - gliosis.

Microscopic

Features:

  • Neurogenic pattern:
    • Group atrophy.
    • +/-Target fibres.

Dermatomyositis

For the skin manifestations see: Inflammatory_skin_disorders#Dermatomyositis.

General

  • Complement mediated disease - membrane attack complex.
  • Usually middle age.
  • Associated skin rash is common.
    • May precede or follow muscle pathology.
  • Associated with malignancy in approximately 10% of cases.[24]

Clinical

  • If the characteristic skin lesions are absent... it is likely idiopathic inflammatory myositis and related to diabetes mellitus.[25]

Microscopic

Features:

  • Perifascicular inflammation with perifascicular atrophy - key feature.
  • Loss of vessels around muscle fibres.
    • Vessels should be where more than 3 or more fibres are opposed to one another.

Images:

EM

  • Endothelial tubuloreticular inclusions (abbrev. TRIs) - undulating tubules in the smooth ER, usu. perinuclear;[26] not pathognomonic - may be seen in inclusion body myositis.[27]

Images:

Inclusion body myositis

General

  • Usually elderly.
  • Thought to be related to Alzheimer's disease due to similar staining with congo red and several IHC stains.[28]

Microscopic

Features:

  • Inflammation.
  • Vacuolated muscle fibres (with proteineous aggregates) key feature.
    • Vacuolation = "inclusion"
      • Usually in the centroidal location.

DDx: polymyositis.

IHC

Features:[28]

  • Congo red +ve.
  • APP +ve, ubiquitin +ve, tau +ve. (???)

EM

  • Inclusion bodies - tubulovescicular material.[29]

Polymyositis

General

  • Tx: steroids.

Microscopic

Features:

  • Inflammation.

DDx: Inclusion body myositis.

Muscular dystrophy

General

  • DDx: large.

A short DDx:

  • Duchenne's muscular dystrophy.[30]
  • Becker's muscular dystrophy.
  • Limb-girdle muscular dystrophy.
    • Lotsa different mutations, autosomal dominant and recessive variants.
  • Myotonic dystrophy.[31][32]

Microscopic

Features:

  • Endomysial fibrosis.
  • Hypercontracted fibres (large muscle fibres).

Images:

Myotonic dystrophy

Microscopic

Features:

  • Internal nuclei/central nuclei.

Nemaline myopathy

General

  • A type of congenital myopathy.
  • Paediatric thingy.

Drug-induced rhabdomyolysis

  • AKA drug-induced acute necrotizing myopathy.

General

Clinical:[33]

  • Myalgias.
  • Myoglobinuria.
  • Increased elevated serum creatine kinase (CK).

Causes:

  • Ecstasy (MDMA).
  • Statins.

Microscopic

Features:

  • Muscle necrosis.
    • Fibre collapse = increased staining on H&E, HPS.
    • Karyolysis - loss of nuclei.
    • Macrophage (phagocytosis) clean-up = pale moth-eaten appearance (seen well on PAS).
  • No inflammation.
  • No perifascicular atrophy.

Images:

Stains

  • PAS +ve fibres (macrophages).

IHC

  • CD45 -ve (no lymphocytes).

EM

Limb-girdle muscular dystrophy

General

  • A group of muscular dystrophies with childhood or adult onset.[34]
  • Rare.
  • Usually autosomal recessive.
  • Treatment: none; supportive only.

Subtypes

  • Sarcoglycanopathy.
  • Calpainopahty.
  • Dysferlinopathy.

Notes:

  • Can be demonstrated with IHC.

DDx

  • DMD gene associated MDs (Duchenne MD, Becker MD).
  • Facioscapulohumeral muscular dystrophy (FSHD).
  • Emery-Dreifuss MD (EDMD).
  • Congenital MD (CMD).
  • Inflammatory myopathies.

Groups of disorders

Mitochondrial disorders

General

  • Onset childhood to adulthood.
  • Heteroplasmy - variable distribution of badness within affected individuals.
    • Leads to "threshold effect".

Microscopic

  • Trichrome most useful - find the ragged red fibres - usu. at the cell periphery.
  • COX-SDH:
    • Non-staining (???).
    • Peripheral blue accumulation in occasional cells.

EM

Features:

  • Crystalloid inclusions.[35]
  • "Ballooned" mitochondria; loss of cristae -- loss of membranous folds within mitochrondrion.

Trichinosis

See Microorganisms.

Parasitic disease classically associated with consumption of uncooked pork.

Type 2 fibre atrophy

General

DDx:

  • Disuse.
  • Space travel.
  • Steroids.
  • Others.

Microscopic

Features:

  • Atrophy for type 2 atrophy.

Images:

Nerve stuff

General

  • Most common biopsy: sural nerve.

Stains

Myelin stain:

  • Blue = myelin.

Gomori trichrome:

  • Axon = green.
  • Myelin = red.

Degenerative changes

Types:[36]

  • Wallerian degeneration.
  • Axonal degeneration.
  • Segmental demyelination.

Wallerian degeneration

  • Digestion chambers - key feature.

Images:

Diseases

  • Guillain–Barré syndrome.
  • Chronic inflammatory demyelinating polyneuropathy (CIDP).[37]
    • Essentially chronic Guillain–Barré syndrome.
  • Toxic polyneuropathy (drug toxicity).[38]

See also

References

  1. ↑ URL: http://moon.ouhsc.edu/kfung/jty1/NeuroHelp/ZNEWWU10.htm. Accessed on: 27 October 2010.
  2. ↑ Filosto M, Tonin P, Vattemi G, et al. (January 2007). "The role of muscle biopsy in investigating isolated muscle pain". Neurology 68 (3): 181–6. doi:10.1212/01.wnl.0000252252.29532.cc. PMID 17224570.
  3. ↑ URL: http://www.gpnotebook.co.uk/simplepage.cfm?ID=1436155929. Accessed on: 27 October 2010.
  4. ↑ URL: http://commons.wikimedia.org/wiki/File:Skeletal_muscle.jpg. Accessed on: 25 October 2010.
  5. ↑ Martini, Frederic H. (2003). Fundamentals of Anatomy & Physiology (6th ed.). Benjamin Cummings. pp. 438. ISBN 978-0805359336.
  6. ↑ URL: http://www.lab.anhb.uwa.edu.au/mb140/corepages/connective/connect.htm. Accessed on: 4 November 2010.
  7. ↑ URL: http://www.lab.anhb.uwa.edu.au/mb140/corepages/muscle/muscle.htm. Accessed on: 28 November 2010.
  8. ↑ URL: http://www.igbmc.fr/recherche/Dep_NG/Eq_JLaporte/JL3.html. Accessed on: 26 October 2010.
  9. ↑ URL: http://www.nature.com/modpathol/journal/v18/n5/full/3800344a.html. Accessed on: 26 November 2010.
  10. ↑ URL: http://nmdinfo.org/lectures/info.php?id=8. Accessed on: 25 October 2010.
  11. ↑ URL: http://neuropathology.neoucom.edu/chapter9/chapter9fALS.html. Accessed on: 25 October 2010.
  12. ↑ URL: http://neuromuscular.wustl.edu/lab/mbiopsy.htm#fibertype. Accessed on: 26 October 2010.
  13. ↑ URL: http://missinglink.ucsf.edu/lm/ids_104_musclenerve_path/student_musclenerve/musclepath.html. Accessed on: 26 October 2010.
  14. ↑ URL: http://moon.ouhsc.edu/kfung/JTY1/Com04/Com401-3-Diss.htm. Accessed on: 28 October 2010.
  15. ↑ URL: http://www.rvc.ac.uk/Research/Labs/NeuroLab/MuscleBiopsy.cfm. Accessed on: 26 October 2010.
  16. ↑ URL: http://neuromuscular.wustl.edu/pathol/dermmyo.htm. Accessed on: 26 October 2010.
  17. ↑ URL: http://neuromuscular.wustl.edu/pathol/ibmpaget.htm. Accessed on: 26 October 2010.
  18. ↑ URL: http://neuromuscular.wustl.edu/pathol/dermmyo.htm. Accessed on: 26 October 2010.
  19. ↑ URL: http://moon.ouhsc.edu/kfung/jty1/neurohelp/ZNEWWU10.htm. Accessed on: 2 March 2011.
  20. ↑ 20.0 20.1 URL: http://moon.ouhsc.edu/kfung/JTY1/Com04/Com401-3-Diss.htm. Accessed on: 28 October 2010.
  21. ↑ URL: http://neuromuscular.wustl.edu/pathol/rod.htm. Accessed on: 26 October 2010.
  22. ↑ URL: http://www.ncbi.nlm.nih.gov/omim/310200. Accessed on: 29 October 2010.
  23. ↑ 23.0 23.1 URL: http://neuromuscular.wustl.edu/pathol/inflammation.htm#cellinv. Accessed on: 3 November 2010.
  24. ↑ Chen YJ, Wu CY, Huang YL, Wang CB, Shen JL, Chang YT (2010). "Cancer risks of dermatomyositis and polymyositis: a nationwide cohort study in Taiwan". Arthritis Res. Ther. 12 (2): R70. doi:10.1186/ar2987. PMC 2888225. PMID 20398365. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2888225/.
  25. ↑ Limaye VS, Lester S, Blumbergs P, Roberts-Thomson PJ (May 2010). "Idiopathic inflammatory myositis is associated with a high incidence of hypertension and diabetes mellitus". Int J Rheum Dis 13 (2): 132–7. doi:10.1111/j.1756-185X.2010.01470.x. PMID 20536597.
  26. ↑ Stoltenburg-Didinger G, Genth E (June 2009). "[Dermatomyositis]" (in German). Z Rheumatol 68 (4): 287–94. doi:10.1007/s00393-008-0398-y. PMID 19330338.
  27. ↑ Katzberg HD, Munoz DG (2010). "Tubuloreticular inclusions in inclusion body myositis". Clin. Neuropathol. 29 (4): 262–6. PMID 20569678.
  28. ↑ 28.0 28.1 Askanas V, Engel WK (November 1995). "New advances in the understanding of sporadic inclusion-body myositis and hereditary inclusion-body myopathies". Curr Opin Rheumatol 7 (6): 486–96. PMID 8579968.
  29. ↑ URL: http://neuromuscular.wustl.edu/pathol/ibm.htm. Accessed on: 3 November 2010.
  30. ↑ URL: http://www.ncbi.nlm.nih.gov/omim/310200. Accessed on: 29 October 2010.
  31. ↑ URL: http://www.ncbi.nlm.nih.gov/omim/160900. Accessed on: 29 October 2010.
  32. ↑ URL: http://www.ncbi.nlm.nih.gov/omim/602668. Accessed on: 29 October 2010.
  33. ↑ Coco, TJ.; Klasner, AE. (Apr 2004). "Drug-induced rhabdomyolysis.". Curr Opin Pediatr 16 (2): 206-10. PMID 15021204.
  34. ↑ URL: http://www.ncbi.nlm.nih.gov/books/NBK1408/. Accessed on: 25 November 2010.
  35. ↑ URL: http://moon.ouhsc.edu/kfung/jty1/neurotest/Q09-Ans.htm. Accessed on: 26 October 2010.
  36. ↑ URL: http://missinglink.ucsf.edu/lm/ids_104_musclenerve_path/student_musclenerve/nervepath.html. Accessed on: 9 November 2010.
  37. ↑ URL: http://path.upmc.edu/cases/case426.html. Accessed on: 14 November 2010.
  38. ↑ URL: http://path.upmc.edu/cases/case173.html. Accessed on: 8 January 2012.

External links

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