ABPath Neuropathology Subspecialty Certification Examination Practice Test
Neuropathology examines diseases of the brain, spinal cord, peripheral nerves, and related structures through tissue morphology, immunohistochemistry, and clinicopathologic correlation. Practice questions sample neurodegenerative disorders, central nervous system tumors, infections, vascular injury, epilepsy-related changes, and spinal cord lesions. These topics involve recognizing patterns of neuronal loss, gliosis, myelin injury, and tumor differentiation.
Exam overview
About the ABPath Neuropathology Subspecialty Certification Examination Exam
Neuropathology work requires connecting anatomic location and histologic pattern with clinical presentation, then selecting findings that distinguish competing diagnoses. Questions may ask you to interpret neuronal and glial changes, identify tumor lineage using markers such as GFAP or PIT1, or relate a loss of protein expression to an underlying molecular alteration. Other tasks include localizing neurologic deficits, recognizing characteristic distributions of infectious encephalitis or ischemia, and distinguishing active inflammation from chronic degeneration or metabolic injury. Practice with these decisions can strengthen pattern recognition across biopsy and resection material, while reinforcing how anatomy, morphology, immunophenotype, and molecular findings contribute to a coherent diagnosis.
Sample Practice Questions
Review a selection from this exam's published US Practice Tests practice bank.
A patient with a slowly progressive movement disorder has neuronal loss and gliosis in the substantia nigra pars compacta. Which additional finding is most characteristic of idiopathic Parkinson disease?
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Correct answer: BIdiopathic Parkinson disease is characterized by loss of dopaminergic neurons in the substantia nigra pars compacta and intraneuronal Lewy bodies and neurites, which are rich in aggregated alpha-synuclein.
A middle-aged adult has progressive memory impairment. The brain shows abundant cortical amyloid plaques and neurofibrillary tangles concentrated in the hippocampus and association cortex. Which protein is the principal component of the neurofibrillary tangles?
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Correct answer: BNeurofibrillary tangles in Alzheimer disease are composed primarily of abnormally phosphorylated tau, a microtubule-associated protein. Amyloid plaques contain amyloid-beta rather than tau.
A circumscribed intramedullary tumor in an adult arises in the cervical spinal cord. Histology shows perivascular pseudorosettes, and tumor cells are GFAP-positive. Which diagnosis is most likely?
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Correct answer: BEpendymomas are common intramedullary spinal cord tumors in adults. Perivascular pseudorosettes, in which tumor cell processes taper toward blood vessels, are a characteristic histologic feature.
A child with a hemispheric mass undergoes resection of a malignant embryonal tumor. Tumor cells show loss of nuclear SMARCB1 (INI1) expression, while internal control cells retain staining. Which molecular event most commonly underlies this immunophenotype?
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Correct answer: ALoss of nuclear INI1 staining in tumor cells with retained staining in internal controls indicates loss of SMARCB1 function. Biallelic inactivation of SMARCB1 is characteristic of atypical teratoid/rhabdoid tumor, among other SMARCB1-deficient neoplasms. Morphology, site, age, and the broader diagnostic context are needed for the final classification.
A patient with fever, headache, and altered mental status has a biopsy showing hemorrhagic necrosis with perivascular lymphocytes in the medial temporal lobe. Which infectious cause is most characteristic of this distribution?
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Correct answer: AHerpes simplex encephalitis classically involves the medial temporal and inferior frontal regions and can produce hemorrhagic necrosis with inflammatory infiltrates. The distribution reflects the virus's characteristic tropism and spread within the brain.
A patient presents with acute unilateral facial weakness involving the forehead and lower face. Which anatomic site is most likely affected when the weakness is peripheral rather than due to a supranuclear lesion?
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Correct answer: AA peripheral-pattern facial palsy can result from injury to the facial nerve nucleus or fascicles in the pons, or to the nerve after it exits the brainstem. It typically weakens both upper and lower facial muscles on the affected side. Supranuclear lesions more often spare much of the forehead because upper facial motor representation receives bilateral corticobulbar input.
A patient with a sellar mass has a pituitary neuroendocrine tumor composed of monomorphic cells with strong nuclear PIT1 expression. The tumor produces growth hormone and prolactin. Which lineage does this immunophenotype support?
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Correct answer: CPIT1 is the lineage-defining transcription factor for somatotroph, lactotroph, and thyrotroph pituitary neuroendocrine tumors. Co-production of growth hormone and prolactin is compatible with a PIT1-lineage tumor. TPIT supports corticotroph differentiation, while SF1 supports gonadotroph differentiation.
How to use this practice test
The free practice bank contains 50 published questions. Each session presents up to 20 questions selected at random, and results appear after the session. Use the questions to identify which neuropathologic patterns or clinicopathologic distinctions need closer review, then revisit those concepts before another session.
Preparation tips
- For neurodegenerative patterns, compare the affected structures and cellular changes, including substantia nigra neuronal loss, gliosis, amyloid plaques, and tau-positive neurofibrillary tangles.
- Practice matching CNS tumor morphology and immunophenotype to lineage; distinguish perivascular pseudorosettes and GFAP expression from molecular clues such as loss of SMARCB1 (INI1).
- Map neurologic findings to anatomy, including peripheral versus supranuclear facial weakness and the spinal cord regions most vulnerable to anterior spinal artery infarction.
- Compare hippocampal sclerosis patterns by documenting neuronal loss and gliosis across CA sectors and the hilus, alongside preservation or involvement of dentate granule cells.
- Review mechanisms and distributions of myelin injury, such as posterior column pallor with relative axonal preservation, and contrast chronic noninflammatory change with active inflammatory lesions.