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Colen Publishing

www.colenpublishing.com

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Colen Publishing, L.L.C.PO Box 36536Grosse Pointe Woods, MI 48236Author and Editor: Chaim B. Colen, M.D., Ph.D.Editorial Assistant: Roxanne E. Colen, PA-C

COPYRIGHT © 2008 by Colen Publishing, L.L.C. This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation without the author’s consent if illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing or duplication of any kind, translating, preparation of microfilms, and electronic data processing and storage.Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain. Permissions may be sought directly from Colen Publishing, L.L.C. by writing to the above address.Printed in ChinaColen Flash-Review: Neurosurgery, 2nd EditionISBNVolume 1: 1-935345-01-X Volume 2: 1-935345-02-8 2 Volume Set: 1-935345-00-1

Note: Knowledge in medicine is constantly changing. The author has consulted sources believed to be reliable in the effort to provide information that is complete and in accord with the standards at the time of publication. However, in view of the possibility of human error by the author in preparation of this work, warrants that the information contained herein is in every respect accurate and complete, and that the author is not responsible for any errors or omissions or for the results obtained from use of such information. The reader is advised to confirm the information contained herein with other sources. This is especially important in connection with new or infrequently used drugs. In such instances, the product information sheet included in the package with each drug should be reviewed.

Colen Publishing

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Glossary

COPYRIGHT-------------------------------------------------- 1PREFACE------------------------------------------------------ 1HOW TO USE THIS CARD REVIEW-------------------- 1CONTRIBUTORS-------------------------------------------- 4GLOSSARY--------------------------------------------------- 1NEUROSURGERY------------------------------------------ 110NEUROLOGY ------------------------------------------------ 86NEUROPATHOLOGY-------------------------------------- 238NEUROANATOMY----------------------------------------- 57NEUROCRITICAL CARE---------------------------------- 80NEURORADIOLOGY--------------------------------------- 73NEUROBIOLOGY------------------------------------------- 64 BONUS BIOSTATISTICS---------------------------------- 6

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Preface• The idea to undertake such a large Flashcard review spawned from watching my wife Roxanne

study for her Physician Assistant Boards. Diligently every day she would create a set of 7-10 flashcards from her study material that she would take with her to work. Later on, when I was studying for my written Neurosurgery Board examination, I gleaned information from various texts and other study guides and wrote down the most relevant material on cards for quick review while at work. It was amazing how much time during the day would be available to review these cards. If there was a delay in a OR case, a long lunch-line, a traffic jam (especially the i94 on a Friday afternoon) or waiting for my wife at her OB/GYN appointment -these little cards were specially handy. Always ambitious in life, the thought of giving this study tool to the busy neurosurgery resident was captivating. My expectation is to enable the resident with a quick yet informative review of basic neuroscience principles. With positive encouragement from my fellow residents on the 1st edition, I cautiously proceed here with updating information, adding new images, improved illustrations and clarification of neuroscience concepts. May this endeavor serve to better our wonderful science inherited through the legacy of Harvey Cushing, Neurosurgery.

Chaim September 9, 2008

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The Colen Flash-Review

Author and EditorChaim B. Colen, M.D., Ph.D.Department of Neurological SurgeryWayne State University School of MedicineDetroit, Michigan

Assistant EditorRoxanne E. Colen, M.S., PA-CColen Publishing, LLCGrosse Pointe, Michigan

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AcknowledgementsI would like to give thanks to a great many wonderful persons whose efforts, although not inscribed in

these cards, were instrumental in making this monumental task possible. One exceptional individual to whom I owe special thanks is my mother in-in-law, Colleen Johns, who babysat my daughter Emily and son Joshua for hours on end, while my wife and I toiled through hundreds of pages of various textbooks and journal articles, formatted questions, and drew computer illustrations. To my daughter Emily Rivka, who incessantly tugged at my pants trying to get my attention to the squirrel in our backyard ;and that big bright smile from my son Joshua that continually sent me optimism. To Mahmoud and Abhi who spent hours at my home assisting with typing, researching and editing; Naomi whose positive attitude in life is exceptionally brightening and uplifted the group’s 2 am brainstorming sessions when I still had to wake up early to work the next day, all the pathologists, especially Doha, who assisted in taking photographs, Dr. William Kupsky, for allowing us access to his collection of unique neuropathology, and to all the medical students especially Kristyn, whose hard work is admirable. There are those whose names are not here but did assist in some way, thank you. I am forever indebted to my training program, the Wayne State University neurosurgery program, my Chairman Dr. Murali Guthikonda, and Associate Chairman Dr. Setti S. Rengachary whose moral support over the last five years has kept me on this educational drive. For this second edition, there were fellow residents that gave me input and new insight that has helped to improve this edition over the first.

To my parents Joseph and Leila, educators of true dedicated quality, and to whom I owe my homeschooling education and self-motivation. Lastly to my wife Roxanne, whose patience with my ambitiousness knows no boundaries.

Thank you All,Chaim September 9, 2008

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How to use this Flashcard review

• These cards are intended to cover most of the aspects of the Neurosurgery Board Examination. They are not a COMPLETE review and therefore they are not intended to replace textbooks. We would advise using these cards during the last couple of weeks before your board exam except for the pathology section which you should go through all year to better remember the photographs in it (heavily encountered during the boards!). BOARD FAVORITEquestions are of extreme importance and most likely to bump into during the boards, so make you sure you know how to answer them right.

• Good luck!• Chaim B. Colen, M.D., Ph.D.

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Faculty Reviewers

Murali Guthikonda, MD Professor and Chairman Department of Neurological SurgeryWayne State University School of MedicineDetroit, Michigan

Setti Rengachary, MD Associate Chairman Department of Neurological SurgeryWayne State University School of MedicineDetroit, Michigan

William, J. Kupsky, MDDepartment of Neuropathology Wayne State University School of MedicineDetroit, Michigan

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• With ever increasing scope and complexity of knowledge base, the current day trainee or practitioner of neurosurgery finds it difficult to keep up with the explosion of neurosurgical information. This is compounded by a healthy growth in specialization in various branches of neurosurgery.

• Chaim has made an attempt to make life simpler by incorporating small quanta of knowledge on flashcards accompanied by clear and simple illustrations. The user may review as few or as many cards as his/her time will allow. Although not meant to be substitutes for standard comprehensive texts and atlases, these cards help to refresh the information learned from the bedside, operating room and standard books. Each card represents a mini-examination with instant access to appropriate answers.

• This is a fun way to recall neurosurgical information especially before an upcoming test.

Setti S. Rengachary, M.D.Department of Neurological Surgery

Forward

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Physician Contributing Authors

Mahmoud Rayes, MDDepartment of Neurological Surgery WSU School of Medicine

Erika Peterson, MDUT Southwestern,Department of Neurological Surgery Dallas, Texas

Rivka R. Colen, MDDepartment of RadiologyThe Massachusetts General HospitalHarvard Medical SchoolBoston, Massachusetts

Doha Itani, MDDepartment of PathologyWSU School of MedicineDetroit, Michigan

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Contributing Medical Students

Darmafall, KristynWayne State UniversitySchool of MedicineClass of 2012

Davis, Naomi Wayne State UniversitySchool of Medicine Class of 2011

Dub, LarissaWayne State UniversitySchool of MedicineClass of 2012

Faulkiner, RodneyWayne State UniversitySchool of MedicineClass of 2012

Galinato, AnthonyWayne State UniversitySchool of MedicineClass of 2012

Gotlib, DorothyWayne State UniversitySchool of MedicineClass of 2009

Kozma, BonitaWayne State UniversitySchool of MedicineClass of 2008

Lai, Christopher Wayne State UniversitySchool of MedicineClass of 2010

Larson, SarahWayne State UniversitySchool of MedicineClass of 2012

Martinez, DerekWayne State UniversitySchool of MedicineClass of 2011

Matthew SmithWayne State UniversitySchool of MedicineClass of 2011

Matto, ShereenWayne State UniversitySchool of MedicineClass of 2012

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Contributing Undergraduates

Jeffrey P. KallasWayne State UniversityClass of 2010

Abhinav KrishnanWayne State UniversityClass of 2010

Peter PaximadisWayne State UniversityClass of 2008

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• This cerebellar specimen is consistent with:

A. Lewy bodyB. Neuritic plaqueC. Kuru plaqueD. Hirano body

NeuropathologyQ?

2

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Neuropathology SectionNeuropathologyA.• The correct answer is C, Kuru plaque.• Pathology of variant Creutzfeldt-Jakob

disease – Kuru demonstrating a “kuru plaque” in cerebellum.

• Accumulation of prion protein PrP in the form of amyloid plaques occurs in some forms of prion disease.

• Hirano bodies (rod-shaped eosin inclusions) are seen in Alzheimer’s disease.

Cerebellum: granular cell layer

PAS

Kuru Plaque

Liberski PP. Amyloid plaques in transmissible spongiform encephalopathies (prion diseases). Folia Neuropathol. 2004;42 Suppl B:109-19. Review.

Cerebellar Infection, Prion, Creutzfeldt-Jakob disease, Kuru, amyloid

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• This brain specimen is most consistent with:

A. Lewy bodyB. Neuritic plaqueC. Kuru plaqueD. Hirano body

NeuropathologyQ?

3

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NeuropathologyA.• The correct answer is D, Hirano body.• Hirano bodies (rod-shaped eosin

inclusions of mostly actin filaments) are seen in Alzheimer’s disease.

• Accumulation of prion protein PrP in the form of amyloid plaques occurs in the pathology of variant Creutzfeldt-Jakob disease – Kuru demonstrates “kuru plaques” in the cerebellum.

• Lewy bodies are seen in Parkinson’s disease and diffuse Lewy body disease. These are formed from α-synuclein.

Kuljis RO: Modular corticocerebral pathology in Alzheimer's disease. In: Mangone CA, Allegri RF, Ariza, eds. Dementia: A Multidisciplinary Approach. 1997: 143-55.

Section of hippocampus

Hirano body

BOARD FAVORITE!

Degenerative disease, Alzheimer’s disease, Hirano bodies

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Used with permission from Handbook of Neurosurgery andNeurology in Pediatrics; By Chaim B. Colen, MD, PhD.

• What is the most likely diagnosis seen in this fundoscopic examination?

A. Drusen bodiesB. Retinopathy of diabetesC. Retinal hemorrhageD. Pseudopapilledema

NeuropathologyQ?

9

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NeuropathologyA.• The correct answer is C, retinal hemorrhages.• Shaken baby syndrome was described by Caffey as a clinical triad: subdural

hematomas, subarachnoid hemorrhages, and retinal hemorrhages.• "Shaken baby syndrome" (SBS) results in intracranial and intraocular hemorrhages

with no evidence of external trauma. The cause of these injuries is vigorous shaking of an infant being held by the chest, shoulders, or extremities.

• Physicians are mandated to report cases of child abuse, elder abuse, sexual abuse, domestic violence, and assault. Physicians are also required to notify the authorities if anyone has a specific plan to commit suicide or homicide.

• Drusen bodies aka “pseudopapilledema” are colloid or hyaline bodies lying beneath the retinal pigment epithelium. They may occur either secondary to changes in the choroid that affect the pigment epithelium or as an autosomal dominant disorder of the retinal pigment epithelium.

Martin HA, Woodson A, Christian CW, Helfaer MA, Raghupathi R, Huh JW. Shaken baby syndrome. Crit Care Nurs Clin North Am. 2006 Sep;18(3):279-86. Review.

Shaken baby syndrome, Pediatrics, Retinal hemorrhages, subdural hematomas,

subarachnoid hemorrhages

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• Which pairing is most accurate for the localization of medulloblastomas in the pediatric and adult population?

A. Children : Midline, Adults : MidlineB. Children : Lateral, Adults : LateralC. Children : Lateral, Adults : MidlineD. Children : Midline, Adults : Lateral

NeuropathologyQ?

54

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Homer-Wright rosette –(pseudorosette) radially arranged nuclei surrounding central fibrillary material (red arrow); histopathological features of medulloblastoma.

NeuropathologyA.• The correct answer is D, children :

midline, adults: lateral

MRI brain -contrast enhanced sagittal image showing the midline location of the tumor in a pediatric patient.

BOARD FAVORITE!

Neoplasm, Cerebellum, PNET, medulloblastoma, location of medulloblastoma, Homer-Wright

rosette

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• Compared to pilocytic astrocytoma:

A. This tumor has a better prognosis

B. This tumor has a similar prognosis.

C. This tumor has a worse prognosis

D. Prognosis is irrelevant

NeuropathologyQ?

114

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NeuropathologyA.• The correct answer is C, this tumor has a worse prognosis..• Gemistocytic astrocytoma is WHO grade II and is distinctive in its appearance, having

astrocytes with generous eosinophilic cytoplasm with a “stuffed” stellate appearance. • Low-grade astrocytomas with a significant fraction of gemistocytes progress more rapidly

and typically carry a p53 mutation.

Krouwer HG, Davis RL, Silver P, Prados M. Gemistocytic astrocytomas: a reappraisal. J Neurosurg. 1991 Mar;74(3):399-406.

Secondary GBMProgenitor cell

pRB loss, NK4α increase, PTEN, loss

Secondary GBM

PDGFR increase

P53 loss

Grade IIastro

Grade IIIastro

BOARD FAVORITE!

neoplasm, astrocytoma, gemistocytic astrocytoma, WHO grade III

Gemistocytic astrocytoma

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• This muscle specimen (Gomori stain) is consistent with which disorder?

A. Myoclonic seizuresB. Disuse atrophyC. Steroid atrophyD. Denervation atrophy

NeuropathologyQ?

138

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NeuropathologyA.• The correct answer is A, myoclonic

seizures.• Mitochondrial disorders (e.g.

MELAS, MERRF) clinically are associated with seizures and muscle biopsy shows ragged-red fibers and rimmed vacuoles.

• Type 1 fiber atrophy- think muscle disease! -myotonic dystrophy and congenital myopathy

• Type 2 muscle atrophy- think neurogenic or muscle disease! –denervation, disuse, myasthenia gravis, steroids and paraneoplastic syndrome (BOARD FAVORITE!)

Fukuhara N, Tokiguchi S, Shirakawa K, Tsubaki T. Myoclonus epilepsy associated with ragged-red fibres (mitochondrial abnormalities ): disease entity or a syndrome? Light-and electron-microscopic studies of two cases and review of literature. J Neurol Sci. 1980 Jul;47(1):117-33.

RAGGED RED FIBERS RIMMED VACUOLE

BOARD FAVORITE!

Muscle, Mitochondrial disease, seizures, ragged-red fibers, rimmed vacuoles, type 1 fiber atrophy,

type 2 fiber atrophy

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• This peripheral nerve biopsy is consistent with:

A. Myasthenia gravisB. Onion bulb formationC. Wallerian degenerationD. Neurofibroma

NeuropathologyQ?

139

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NeuropathologyA.• The correct answer is B, onion bulb

formation.• Onion bulb formation occurs

after repeated cycles of demyelination and remyelination result in a thick layer of abnormal myelin around the peripheral axons. These changes cause what is referred to as an onion bulb appearance.

• May be seen in a few disorders: Charcot-Marie-Tooth (CMT) and Refsum’s disease (phytanic acid disorder).

Bornemann A, Hansen FJ, Schmalbruch H: Nerve and muscle biopsy in a case of hereditary motor and sensory neuropathy type III with basal lamina onion bulbs. Neuropathol Appl Neurobiol 1996 Feb; 22(1): 77-81.

ONION BULBSONION BULB (electron microscopy)

BOARD FAVORITE!

Peripheral nerve, Onion bulb formation, myelin, Charcot-Marie-Tooth, Refsum’s disease

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• Symptoms of a patient with this diagnosis might be alleviated with which of the following drugs:

A. Retroviral drugB. Anticholinesterase inhibitorC. Beta-interferonD. Trimethoprim-

sulfamethoxazole

NeuropathologyQ?

140

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NeuropathologyA.• The correct answer is A,

anticholinesterase inhibitor.• Microscopy shows an amyloid

plaque and neurofibrillary tangles that would be consistent with the diagnosis of Alzheimer’s disease.

• Donepezil is a synthetic noncovalent reversible inhibitor of acetylcholinesterase (AChE) for the treatment of mild to moderate dementia associated with Alzheimer's disease.

• Other drugs include galantamine and rivastigmine.

Kuljis RO: Modular corticocerebral pathology in Alzheimer's disease. In: Mangone CA, Allegri RF, Ariza, eds. Dementia: A Multidisciplinary Approach. 1997: 143-55.

Neurofibrillary tangle

Amyloid plaque

Degenerative disease, Dementia, Alzheimer’s disease, neurofibrillary tangles, amyloid plaque,

Donepezil, Acetylcholinesterase inhibitor

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• This brain specimen is most consistent with:

A. Alzheimer’s diseaseB. Parkinson’s diseaseC. Pick’s diseaseD. Wilson’s disease

NeuropathologyQ?

142

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NeuropathologyA.• The correct answer is B,

Parkinson’s disease.• Microscopy shows melanophages

and neuronal cell loss in the substantia nigra pars compacta.

• Lewy bodies are also seen. These are formed from α-synuclein.

• Pick bodies are seen in Pick’s disease using silver stain.

Hodaie M, Neimat JS, Lozano AM. The dopaminergic nigrostriatal system and Parkinson's disease: molecular events in development, disease, and cell death, and new therapeutic strategies. Neurosurgery. 2007 Jan;60(1):17-28; discussion 28-30.

NEURONAL LOSS LEWY BODY

BOARD FAVORITE!

Degenerative disease, Movement disorder, Parkinson’s disease, melanophages, lewy bodies,

alpha-synuclein

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• This neonatal brain specimen is consistent with which hemorrhage grade?

A. Grade IB. Grade IIC. Grade IIID. Grade IV

NeuropathologyQ?

148

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NeuropathologyA.• The correct answer is C, grade III.• This gross specimen demonstrates germinal matrix

hemorrhage (GMH) and intraventricular hemorrhage (IVH) and hydrocephalus which are the most common and most important neurologic injuries in preterm neonates.

• Premature infants lack the ability to autoregulate the cerebral blood pressure. Fluctuations in cerebral blood pressure and flow can rupture the primitive germinal matrix vessels or lead to infarction of the metabolically active germinal matrix. Neurologic sequelae, include cerebral palsy, mental retardation, and seizures.

Levy ML, Masri LS, McComb JG: Outcome for preterm infants with germinal matrix hemorrhage and progressive hydrocephalus. Neurosurgery 1997 Nov; 41(5): 1111-7; discussion 1117-8.

GRADE 3

IVH and hydrocephalus

GMH

Grading SystemGrade 1 - confined GMHGrade 2 - IVH without hydrocephalus.Grade 3 - IVH with associated hydrocephalusGrade 4 - Intraparenchymal hemorrhage

BOARD FAVORITE!

Vasculature, hemorrhage, hemorrhage grading, germinal matrix hemorrhage, intraventricular

hemorrhage, Pediatrics

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• This pathology is most likely due to:

A. Vitamin A toxicityB. Cyanocobalamine

deficiency C. Thiamine deficiencyD. Vitamin B6 deficiencyE. Alcohol intake

NeuropathologyQ?

149

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NeuropathologyA.• The correct answer is C, thiamine

deficiency.• Thiamine deficiency is seen in chronic

malnourished alcoholics. Note the old infarction that has occurred in the mamillary bodies.

• Wernicke-Korsakoff’s syndrome –subacute amnesia seen in damage to the mamillary bodies and may be caused by thiamine deficiency and may be reversible with the administration of thiamine.

Torvik A. Topographic distribution and severity of brain lesions in Wernicke's encephalopathy. Clin Neuropathol. 1987 Jan-Feb;6.

Old infarction

BOARD FAVORITE!

Nutritional deficiency, Thiamine deficiency, Wernicke-Korsakoff syndrome, mamillary bodies

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• This brain specimen is most consistent with which disease?

A. Wilson’s (hepatolenticular degeneration)

B. Alzheimer’sC. Pick’sD. Parkinson’sE. Huntington’s

NeuropathologyQ?

151

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NeuropathologyA.• The correct answer is A, Wilson's disease

(hepatolenticular degeneration). • Wilson’s disease is caused by accumulation

of copper in the brain with decreased serum copper and ceruloplasmin and increased urine copper. Kayser-Fleischer rings form around the iris.

• Microscopy demonstrates Alzheimer type 2 astrocytes which have a large clear vesicular nuclei and prominent nucleoli. Proliferation of large protoplasmic astrocytes such as Opalski cells may be seen.

• Research suggests that these reactive astrocytes may be involved in the process of copper detoxification in WD.

Bertrand E, Lewandowska E, Szpak GM, Hoogenraad T, Blaauwgers HG, Czlonkowska A, Dymecki J. Neuropathological analysis of pathological forms of astroglia in Wilson's disease. Folia Neuropathol. 2001;39(2):73-9.

BOARD FAVORITE!

Degenerative disease, Wilson’s disease, Alzheimer type 2 astrocytes, Opalski cells,

Copper

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• This muscle biopsy specimen is consistent with:

A. Congenital myopathyB. Myotonic dystrophyC. Steroid myopathyD. Mitochondrial myopathy

Note: Type 1 fibers labeled (1).

NeuropathologyQ?

152

1

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NeuropathologyA.• The correct answer is C, steroid myopathy.• Steroid myopathy is characterized by

type 2 myofiber atrophy!

• Type 1 fiber atrophy- think muscle disease! -myotonic dystrophy and congenital myopathy

• Type 2 muscle atrophy- think neurogenic or muscle disease! –denervation, disuse, myasthenia gravis, steroids and paraneoplastic syndrome (BOARD FAVORITE)

STEROID MYOPATHY

TYPE 2 ATROPHY

Griggs RC, Mendell JR, Miller RG: Congenital myopathies. In: Evaluation and Treatment of Myopathies. Philadelphia: FA Davis Co; 1995: 211-46.

BOARD FAVORITE!

Muscle, myopathy, steroid myopathy, type 2 fiber atrophy

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• This gross brain specimen is most consistent with:

A. AdrenoleukodystrophyB. Multiple sclerosisC. Mitochondrial myopathyD. Canavan’s disease

NeuropathologyQ?

154

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NeuropathologyA.• The correct answer is B, multiple sclerosis.• Multiple sclerosis (MS) is an idiopathic

(autoimmune?) inflammatory demyelinating disease of the CNS. Animal model experimental allergic encephalomyelitisdemonstrated by autoimmunity to myelin basic proteins. (BOARD FAVORITE)

• Episodes of de/remyelination result in a chronic burned-out plaque with relative preservation of axons and gliosis (recently axon transection has been reported in acute exacerbations).

• Incidence is higher in Caucasians. Female-to-male ratio is 2:1.

• Classic presentation -optic neuritis, transverse myelitis, internuclear ophthalmoplegia, paresthesias

Noseworthy JH, Lucchinetti C, Rodriguez M, Weinshenker BG: Multiple sclerosis. N Engl J Med 2000 Sep 28; 343(13): 938-52.

Periventricular location

Chronic plaques

BOARD FAVORITE!

Demyelinating disease, Inflammatory disease, Multiple Sclerosis, myelin basic protein

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• The gross spinal cord specimen (A) is most consistent with:

A. AdrenoleukodystrophyB. Multiple sclerosisC. Amyotrophic lateral sclerosisD. Neurofibromatosis

NeuropathologyQ?

A B

156

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Neuropathology

A B

A.• The correct answer is C, amyotrophic

lateral sclerosis.• Amyotrophic lateral sclerosis

progressive loss of upper and lower motor neurons.

• Pathology: progressive loss of anterior horn cells leads to atrophy of ventral nerve fibers and of skeletal muscles; progressive loss of primary motor neurons in motor cortex leads to degeneration of corticospinal/ corticobulbar tracts.

• Adrenoleukodystrophy (ALD)-leukodystrophy is an x-linked recessive disease due to deficiency in peroxisomal lipid oxidation.

Gartner J, Braun A, Holzinger A , et al: Clinical and genetic aspects of X-linked adrenoleukodystrophy. Neuropediatrics 1998 Feb; 29(1): 3-13.

Ventral nerve root atrophy

BOARD FAVORITE!

Normal ventral roots

spinal cord, Degenerative disease, Amyotrophic lateral sclerosis, Upper motor neuron, Lower

motor neuron

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• This gross brain specimen shows atrophy that is consistent with:

A. Multiple sclerosisB. Pick’s diseaseC. Alzheimer’s diseaseD. Acute cerebral infarction

NeuropathologyQ?

157

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NeuropathologyA.• The correct answer is Alzheimer’s

disease.• Alzheimer’s disease is the most

common dementing illness in adults, characterized by progressive dementia over several years. There is increased frequency with increasing age and in familial cases, usually earlier onset.

• Note the diffuse brain atrophy of Alzheimer's disease, unlike Pick’s disease which has mostly frontal lobe atrophy.

• Risk is increased in Down’s syndrome (BOARD FAVORITE). Kuljis RO: Modular corticocerebral pathology in Alzheimer's disease. In: Mangone CA,

Allegri RF, Ariza, eds. Dementia: A Multidisciplinary Approach. 1997: 143-55.

Frontal Atrophy

Temporal Atrophy

BOARD FAVORITE!

Degenerative disease, Alzheimer’s disease, dementia, diffuse atrophy

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• The pathology seen here is most likely due to:A. Cerebellar astrocytomaB. AlcoholismC. TraumaD. Ruptured aneurysmE. Arteriovenous malformation

NeuropathologyQ?

158

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NeuropathologyA.• The correct answer is….• To obtain the answer to this question and to

view over 400 more comprehensive pathology questions please purchase the full product here!

Bolla L, Palmer RM: Paraneoplastic cerebellar degeneration. Case report and literature review. Arch Intern Med 1997 Jun 9; 157(11): 1258-62.

BOARD FAVORITE!

Degeneration, Cerebellum, Alcohol related degeneration, superior vermis of cerebellum