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Free Practice Questions for Iraqi Board Neurology

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Key Facts: Iraqi Board Neurology Exam

IBMS / MOHESR

Governing Body & Ministry

Iraqi Board for Medical Specializations

5 Years

Residency Training Duration

IBMS Neurology Curriculum 2025

60%

Published Pass Mark (Final Written & Clinical)

Scientific Council of Neurology curriculum

100 MCQs

Practice Bank Study Items

OpenExamPrep

The Iraqi Board of Neurology (IBMS/MOHESR) qualification involves a 5-year residency assessed by the Part 1 Written Exam (basic neurosciences and internal medicine; 60% pass mark, max 4 attempts), the Final Written Exam (100 MCQs; 60% pass mark, max 4 attempts), and the Final Clinical/Oral Exam (long case, 3 short cases, viva; 60% pass mark), alongside an approved research dissertation. This independent 100-question MCQ practice bank supports preparation for the theoretical written knowledge base of Part 1 and Part 2; it is not a clinical OSCE simulation or a substitute for accredited hospital residency training.

Sample Iraqi Board Neurology Practice Questions

Try these sample questions to review concepts for the Iraqi Board Neurology exam. Each question includes a detailed explanation. Start the interactive quiz above for the full 100+ question experience with AI tutoring.

1A 58-year-old man presents with sudden-onset severe vertigo, nausea, dysphagia, hoarseness, and ataxia. Neurological examination reveals right-sided Horner syndrome, right facial sensory loss to pinprick, right cerebellar dysmetria, and diminished pinprick sensation over the left arm and leg. Motor strength is 5/5 bilaterally. Occlusion of which artery is most commonly responsible for this clinical syndrome?
A.Posterior inferior cerebellar artery (PICA)
B.Anterior inferior cerebellar artery (AICA)
C.Superior cerebellar artery (SCA)
D.Paramedian branch of the basilar artery
Explanation: This patient presents with lateral medullary syndrome (Wallenberg syndrome), most frequently caused by atherothrombotic occlusion of the vertebral artery or the posterior inferior cerebellar artery (PICA). The constellation of findings reflects infarction of lateral medullary structures: nucleus ambiguus (dysphagia, hoarseness), descending sympathetic tract (ipsilateral Horner syndrome), spinal trigeminal nucleus/tract (ipsilateral facial pain/temperature loss), inferior cerebellar peduncle (ipsilateral ataxia), and spinothalamic tract (contralateral body pain/temperature loss). Corticospinal fibers run ventrally in the medullary pyramid and are characteristically spared, preserving motor power.
2A 66-year-old hypertensive woman develops sudden-onset complete ptosis and pupillary dilation of the left eye with an eye that rests 'down and out'. Concurrently, she has a dense right-sided hemiplegia affecting the face, arm, and leg. Which brainstem vascular syndrome does this presentation represent?
A.Weber syndrome
B.Benedikt syndrome
C.Claude syndrome
D.Foville syndrome
Explanation: Weber syndrome is an anterior (ventral) midbrain stroke syndrome typically resulting from occlusion of penetrating branches of the posterior cerebral artery or top of the basilar artery. It is characterized by an ipsilateral third nerve palsy (due to involvement of oculomotor fascicles) and contralateral upper motor neuron hemiplegia (due to involvement of the cerebral peduncle / descending corticospinal and corticobulbar tracts).
3A 32-year-old woman with relapsing-remitting multiple sclerosis presents with diplopia during horizontal gaze. Examination reveals that on attempted conjugate rightward gaze, her left eye fails to adduct across the midline, while her right eye abducts fully with horizontal jerk nystagmus. Convergence of both eyes is intact. What is the precise anatomical localization of the causative lesion?
A.Left medial longitudinal fasciculus (MLF)
B.Right medial longitudinal fasciculus (MLF)
C.Left paramedian pontine reticular formation (PPRF)
D.Right abducens (CN VI) nucleus
Explanation: This patient exhibits a left internuclear ophthalmoplegia (INO), localized to the left medial longitudinal fasciculus (MLF). The MLF coordinates horizontal conjugate gaze by carrying internuclear axons from the contralateral abducens nucleus (in the pons) to the ipsilateral oculomotor nucleus (in the midbrain) for medial rectus activation. Impaired adduction of the left eye indicates disruption of the left MLF, while the abducting right eye exhibits dissociated nystagmus. Convergence remains preserved because the convergence pathway bypasses the MLF.
4A 24-year-old man suffers a penetrating stab wound to the back, resulting in a clean anatomical hemisection of the right thoracic spinal cord at the T10 level (Brown-Séquard syndrome). Which neurological deficit pattern is expected below the level of the injury?
A.Right-sided spastic weakness and vibration loss, with left-sided pain and temperature sensory loss
B.Left-sided spastic weakness and vibration loss, with right-sided pain and temperature sensory loss
C.Bilateral spastic paraparesis with preserved light touch sensation
D.Right-sided loss of pain and temperature, with left-sided loss of joint position sense
Explanation: Spinal cord hemisection (Brown-Séquard syndrome) damages uncrossed ascending pathways (dorsal columns: vibration and proprioception) and descending motor pathways (lateral corticospinal tract: motor strength), producing ipsilateral upper motor neuron weakness and loss of vibration/position sense below the lesion level. In contrast, second-order spinothalamic fibers cross the anterior white commissure 1 to 2 segments above their entry level to ascend in the contralateral cord, producing loss of pain and temperature sensation on the contralateral side below the lesion.
5A 45-year-old man presents with acute right facial weakness. On examination, he cannot wrinkle his right forehead, close his right eye completely, or elevate the right angle of his mouth. Taste on the anterior two-thirds of his tongue is also impaired. What neuroanatomical feature explains why a cerebral cortical stroke typically spares the upper facial muscles, unlike this patient's lesion?
A.Bilateral supranuclear (corticonuclear) innervation of the motor neurons supplying the upper face
B.Exclusive sensory innervation of the frontalis muscle by the trigeminal ophthalmic branch (V1)
C.Ipsilateral corticonuclear innervation of the upper face and contralateral innervation of the lower face
D.Decussation of facial motor nerve fibers at the level of the midbrain instead of the pons
Explanation: The facial motor nucleus in the lower pons is organized somatotopically: the subnucleus supplying upper facial muscles (frontalis and orbicularis oculi) receives bilateral corticonuclear (corticobulbar) projections from both cerebral motor cortices. Consequently, a unilateral supranuclear upper motor neuron (UMN) lesion (e.g., stroke) spares forehead wrinkling due to compensatory contralateral cortical drive. In contrast, a lower motor neuron (LMN) lesion of the facial nerve fascicle or peripheral trunk (as in Bell palsy) abolishes input to all ipsilateral facial muscles, causing complete hemifacial paralysis including the forehead.
6A 28-year-old man with pharmacoresistant temporal lobe epilepsy undergoes an anterior temporal lobectomy. Postoperatively, automated perimetry reveals a dense visual field defect described as a contralateral superior homonymous quadrantanopia ('pie in the sky'). Disruption of which anatomical white matter bundle is responsible for this deficit?
A.Meyer loop (ventral optic radiations looping through the temporal lobe)
B.Baum loop (dorsal optic radiations traversing the parietal lobe)
C.Main optic tract passing through the retro-lenticular internal capsule
D.Calcarine fissure striate cortex superior bank
Explanation: Meyer loop consists of optic radiation fibers originating in the lateral geniculate nucleus that represent the superior contralateral visual field quadrant (derived from the inferior retinal quadrants). These fibers loop anteroinferiorly around the anterior tip of the temporal horn of the lateral ventricle before traveling back to the inferior bank of the calcarine fissure (lingual gyrus). Damage to Meyer loop during anterior temporal lobe resections or temporal infarctions causes a contralateral superior homonymous quadrantanopia ('pie in the sky').
7A 16-year-old boy presents with progressive morning headaches, morning nausea, and blurry vision. Examination reveals paralysis of upward conjugate gaze, convergence-retraction nystagmus on attempted upward saccades, bilateral eyelid retraction (Collier sign), and pupils that respond briskly to near accommodation but react poorly to direct light. What is the most likely location of the underlying mass lesion?
A.Pineal region compressing the dorsal midbrain tegmentum
B.Pituitary fossa compressing the optic chiasm
C.Cerebellopontine angle compressing the seventh and eighth cranial nerves
D.Foramen magnum compressing the cervicomedullary junction
Explanation: This patient demonstrates the classic features of Parinaud syndrome (dorsal midbrain syndrome), characteristically produced by pineal gland tumors (such as germinomas or pineocytomas) compressing the superior colliculi and pretectal area of the rostral dorsal midbrain. The syndrome features supranuclear upgaze palsy (injury to the rostral interstitial nucleus of the MLF / posterior commissure), convergence-retraction nystagmus, light-near pupillary dissociation (pretectal damage sparing ventral accommodative fibers), and bilateral upper lid retraction (Collier sign).
8During the propagation of a neuronal action potential, what biophysical mechanism is primarily responsible for the absolute refractory period?
A.Inactivation of voltage-gated sodium channels
B.Slow closing of voltage-gated potassium channels
C.Activation of the sodium-potassium ATPase pump
D.Opening of ligand-gated chloride channels
Explanation: The absolute refractory period occurs immediately after the peak of the action potential upstroke, during which no stimulus, regardless of intensity, can elicit a second action potential. This is governed by the time- and voltage-dependent closure of the inactivation gates ('ball-and-chain' mechanism) of voltage-gated sodium channels. Until the membrane repolarizes sufficiently to allow sodium channels to transition from the inactivated state back to the resting closed state, depolarization cannot occur.
9At the neuromuscular junction, what molecular event triggers the exocytosis of acetylcholine quanta from presynaptic synaptic vesicles into the synaptic cleft?
A.Calcium influx via presynaptic P/Q-type voltage-gated calcium channels
B.Sodium influx via presynaptic Nav1.4 voltage-gated sodium channels
C.Potassium efflux through presynaptic Kv1.1 potassium channels
D.Direct mechanical opening of presynaptic SNARE complexes by ATP hydrolysis
Explanation: Depolarization of the presynaptic motor nerve terminal opens presynaptic P/Q-type voltage-gated calcium channels (VGCCs). The resulting rapid influx of Ca2+ elevates local microdomain calcium concentrations, which binds to synaptotagmin-1. Synaptotagmin triggers conformational zippering of the SNARE protein complex (syntaxin-1, SNAP-25, and synaptobrevin), inducing fusion of synaptic vesicle membranes with the presynaptic plasma membrane and quantal release of acetylcholine.
10A 68-year-old man undergoes repair of a thoracoabdominal aortic aneurysm. On waking from anesthesia, he has dense flaccid paraplegia and bilateral loss of pain and temperature sensation below the T6 dermatome, with urinary retention. However, his joint position and vibration sensations remain entirely intact in both lower extremities. What vascular territory has been compromised?
A.Anterior spinal artery
B.Posterior spinal arteries
C.Artery of Adamkiewicz supplying posterior columns only
D.Posterior inferior cerebellar artery descending branches
Explanation: Anterior spinal artery syndrome results from ischemia in the anterior two-thirds of the spinal cord, frequently following cross-clamping of the descending aorta or sacrifice of intercostal/lumbar radicular arteries (including the great radicular artery of Adamkiewicz). The anterior spinal artery supplies the anterior horns (causing flaccid lower motor neuron weakness acutely), lateral corticospinal tracts (bilateral motor paraplegia), and lateral spinothalamic tracts (loss of pain and temperature). The dorsal columns (fasciculus gracilis and cuneatus) are supplied by the dual posterior spinal arteries and are characteristically spared, preserving vibration and proprioception.

About the Iraqi Board Neurology Exam

The Fellowship of the Iraqi Board for Medical Specializations in Neurology (F.I.B.M.S.) is the definitive postgraduate professional qualification for clinical neurologists in Iraq, awarded by the Iraqi Board for Medical Specializations (IBMS) under the Ministry of Higher Education and Scientific Research (MOHESR). The five-year residency program trains physicians in comprehensive neurological consultation, neurocritical care, stroke interventions, clinical electrophysiology (EEG, EMG, nerve conduction studies, evoked potentials), neuroimaging interpretation, and neurogenetics. Important disclosure: The complete FIBMS qualification requires accredited clinical residency training, clinical procedures, research dissertation defense, bedside long-case examinations, short-case clinical stations, and oral viva voce assessments, none of which can be simulated by multiple-choice questions alone. This 100-question multiple-choice practice bank is an independent English-language educational study resource designed to reinforce theoretical knowledge, neuroanatomical localization, diagnostic reasoning, and evidence-based pharmacotherapy for the Part 1 and Final written examinations. It is not an official IBMS examination, does not provide OSCE or clinical viva evaluations, and is not a substitute for formal accredited clinical residency training.

Exam sponsor: Scientific Council of Neurology, Iraqi Board for Medical Specializations (المجلس العراقي للاختصاصات الطبية — المجلس العلمي لاختصاص طب الجملة العصبية). The requirements and fees below concern the certification or admission exam, separate from our free practice resources.

Assessment

The Iraqi Board in Neurology is a five-year structured postgraduate medical residency administered by the Scientific Council of Neurology under the Iraqi Board for Medical Specializations (IBMS) and the Ministry of Higher Education and Scientific Research (MOHESR). The assessment pathway comprises: 1) Part 1 Written Examination, sat after completion of the first year (internal medicine and basic neurosciences: neuroanatomy, neurophysiology, neuropathology, neurogenetics, and neuropharmacology; pass mark is 60%; maximum of 4 examination attempts permitted). 2) Final Written Examination, held annually at the conclusion of training, consisting of a written paper containing 100 single-best-answer MCQs covering adult and pediatric clinical neurology, neurophysiology (EEG, EMG/NCS), neuroradiology, and therapeutics (pass mark is 60%; maximum of 4 attempts allowed, not exceeding twice the training duration). 3) Final Clinical and Oral Examination, taken upon successfully passing the Final Written Examination, consisting of a Long Case (1 hour: 30 minutes clinical history/examination and 30 minutes committee discussion; pass mark 60%), three Short Cases (pass mark 60%), and an Oral Viva Voce examination (pass mark 60%), with an overall clinical pass threshold of 60%. 4) Completion and formal defense of an approved clinical research dissertation.

Time Limit

Typically 2.5 to 3 hours for written examination papers

Passing Score

The Scientific Council of Neurology publishes a pass mark of 60 for the final written paper, and 60% for each of the long case, short cases and oral components of the clinical examination. Part 1 is run by the faculty of internal medicine according to that council's system, so the neurology council does not publish its own Part 1 pass mark.

Exam / Certification Fees

Prescribed by Iraqi Board for Medical Specializations / MOHESR regulatory bylaws

Exam sponsor website

Reported exam pass rate: 60% (final written paper). The Scientific Council of Neurology publishes a pass mark of 60 for the final written paper, and 60% for each of the long case, short cases and oral viva in the clinical examination. Passing the final written paper is a prerequisite for sitting the clinical and oral examination. Part 1 is run by the faculty of internal medicine according to that council's system, so the neurology council does not publish a Part 1 pass mark of its own. This describes exam candidates, not OpenExamPrep users or results from using our resources. Exam sponsor website

Fees, eligibility, and exam policies can change. Confirm them with the exam sponsor before applying or paying.

Our practice resources: topics covered

We aim to reflect publicly available exam outlines and topic information in our study resources. Coverage, format, and difficulty may differ from the actual exam, and we cannot guarantee that every detail is accurate or current. Confirm exam requirements, fees, and policies with the official exam sponsor.

20%

Neuroanatomy, Neurophysiology, Neurogenetics & Neuropathology

Brainstem cross-sectional anatomy, cranial nerve nuclei, ascending and descending spinal pathways, circle of Willis vascular territories, synaptic physiology, ion channelopathies, neuromuscular junction electrophysiology, hereditary neurological disorders, and histopathological hallmarks of central and peripheral nervous system diseases.

25%

Cerebrovascular Disease & Stroke Medicine

Pathophysiology and localization of ischemic stroke syndromes, indications and contraindications for IV thrombolysis (alteplase/tenecteplase), endovascular thrombectomy selection criteria (ASPECTS score, perfusion mismatch), acute blood pressure targets, intracerebral hemorrhage management, aneurysmal subarachnoid hemorrhage complications (vasospasm, hydrocephalus), cerebral venous sinus thrombosis, and antithrombotic regimens for secondary stroke prevention.

20%

Epilepsy, Sleep Disorders & Clinical Neurophysiology

2017 ILAE seizure classification, emergency management of convulsive and non-convulsive status epilepticus, antiseizure medication pharmacology and adverse effects (teratogenicity, cutaneous reactions, pharmacokinetic interactions), electroencephalography (normal rhythms, focal spikes, generalized spike-wave discharges, encephalopathic patterns), electromyography/nerve conduction studies (axonal vs demyelinating neuropathy, decremental response), and primary sleep disorders (narcolepsy, REM sleep behavior disorder).

18%

Movement Disorders, Dementia & Behavioral Neurology

Parkinson disease diagnosis and pharmacotherapy (levodopa, dopamine agonists, MAO-B/COMT inhibitors), atypical parkinsonian disorders (progressive supranuclear palsy, multiple system atrophy, corticobasal degeneration, dementia with Lewy bodies), tremor syndromes, chorea and Huntington disease, dystonia, Wilson disease diagnosis and copper chelation, Alzheimer disease biomarkers and treatment, frontotemporal lobar degeneration, and normal pressure hydrocephalus.

17%

Neuroimmunology, Neuromuscular & Neurological Infections

Multiple sclerosis diagnosis (2017 McDonald criteria) and disease-modifying therapies, neuromyelitis optica spectrum disorder (anti-AQP4) and MOGAD, acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré syndrome) and variants, myasthenia gravis (anti-AChR, anti-MuSK) and myasthenic crisis, amyotrophic lateral sclerosis (ALS), acute community-acquired and nosocomial bacterial meningitis, herpes simplex encephalitis, CNS tuberculosis, and neurobrucellosis.

Preparing for the Iraqi Board Neurology Exam

What You Need to Know

  • Passing score: The Scientific Council of Neurology publishes a pass mark of 60 for the final written paper, and 60% for each of the long case, short cases and oral components of the clinical examination. Part 1 is run by the faculty of internal medicine according to that council's system, so the neurology council does not publish its own Part 1 pass mark.
  • Assessment: The Iraqi Board in Neurology is a five-year structured postgraduate medical residency administered by the Scientific Council of Neurology under the Iraqi Board for Medical Specializations (IBMS) and the Ministry of Higher Education and Scientific Research (MOHESR). The assessment pathway comprises: 1) Part 1 Written Examination, sat after completion of the first year (internal medicine and basic neurosciences: neuroanatomy, neurophysiology, neuropathology, neurogenetics, and neuropharmacology; pass mark is 60%; maximum of 4 examination attempts permitted). 2) Final Written Examination, held annually at the conclusion of training, consisting of a written paper containing 100 single-best-answer MCQs covering adult and pediatric clinical neurology, neurophysiology (EEG, EMG/NCS), neuroradiology, and therapeutics (pass mark is 60%; maximum of 4 attempts allowed, not exceeding twice the training duration). 3) Final Clinical and Oral Examination, taken upon successfully passing the Final Written Examination, consisting of a Long Case (1 hour: 30 minutes clinical history/examination and 30 minutes committee discussion; pass mark 60%), three Short Cases (pass mark 60%), and an Oral Viva Voce examination (pass mark 60%), with an overall clinical pass threshold of 60%. 4) Completion and formal defense of an approved clinical research dissertation.
  • Time limit: Typically 2.5 to 3 hours for written examination papers
  • Exam / certification fees: Prescribed by Iraqi Board for Medical Specializations / MOHESR regulatory bylaws Official sources

Using Our Practice Resources

  • Work through all 100 available questions
  • Review every answer and explanation
  • Track weak areas and revisit them
  • Use our AI tutor for tough concepts

Iraqi Board Neurology: Suggested Study Strategy

1Master neuroanatomical localization: always determine whether the clinical deficit localizes to the cerebral cortex, subcortical white matter, brainstem, spinal cord tract, anterior horn cell, peripheral nerve, neuromuscular junction, or muscle before selecting diagnostic investigations.
2Know acute ischemic stroke protocols by heart: memorize time windows for IV thrombolysis (0 to 4.5 hours), blood pressure thresholds (<185/110 mmHg prior to thrombolysis, <180/105 mmHg for 24 hours post-infusion), and key exclusion criteria including active bleeding or recent major surgery.
3Differentiate status epilepticus phases: memorize the sequential treatment protocol—first-line IV lorazepam/diazepam/midazolam within 5 to 10 minutes, second-line IV levetiracetam, fosphenytoin, or valproate sodium, and third-line continuous IV infusions (propofol, midazolam, or ketamine) for refractory status epilepticus.
4Understand clinical neurophysiology principles: recognize characteristic EEG patterns (3 Hz spike-and-wave in childhood absence, triphasic waves in hepatic/metabolic encephalopathy, periodic lateralized epileptiform discharges [LPDs] in HSV encephalitis) and EMG/NCS findings (conduction block and prolonged F-latencies in demyelinating polyneuropathy vs reduced amplitudes in axonal loss).
5Memorize diagnostic criteria for neuroimmunological and movement disorders: 2017 McDonald criteria for multiple sclerosis, anti-AQP4 testing for NMOSD, cardinal signs of Parkinson disease, and the distinguishing clinical 'red flags' of atypical parkinsonian syndromes (early falls in PSP, early severe dysautonomia in MSA, alien limb in CBD).

Frequently Asked Questions

What is the governing authority and credential awarded by the Iraqi Board in Neurology?

The Iraqi Board of Neurology is administered by the Scientific Council of Neurology (المجلس العلمي لاختصاص طب الجملة العصبية) under the Iraqi Board for Medical Specializations (IBMS / المجلس العراقي للاختصاصات الطبية), which operates under the Ministry of Higher Education and Scientific Research (MOHESR). Successful trainees are awarded the Fellowship of the Iraqi Board for Medical Specializations (F.I.B.M.S.) in Neurology, the recognized benchmark for clinical neurology specialist practice in Iraq.

What is the examination structure and timeline for the Iraqi Board of Neurology?

The 5-year curriculum has two major examination stages: 1) Part 1 Written Examination, sat after completion of the first year, focusing on basic neurosciences (neuroanatomy, neurophysiology, neuropathology, neurogenetics, neuropharmacology) and core internal medicine. 2) Final Examination, taken at the end of the fifth year, consisting of a 100-MCQ Final Written Examination followed by a Clinical and Oral Examination (a 1-hour long case, three short cases, and an oral viva voce examination). In addition, residents must complete and defend a scientific research dissertation before clinical qualification.

What are the passing criteria and retake limits for the written and clinical examinations?

The published pass mark for the final written paper is 60, and each clinical component (long case, short cases and oral viva) also requires 60%. Part 1 is run by the faculty of internal medicine according to that council's system, so the neurology council does not publish a separate Part 1 pass mark. Candidates are allowed a maximum of four attempts at the Part 1 written examination, provided the last attempt does not exceed twice the training duration, and up to four attempts at the final written examination, which is held once a year. Passing the written paper is mandatory before appearing for the clinical and oral examination.

In what language are the Iraqi Board neurology written and clinical examinations conducted?

The Iraqi Board for Medical Specializations publishes this council's curriculum, syllabus and reference list in English, and English-language proficiency appears among the admission requirements set by the Ministry. The council's published curriculum does not, however, contain any statement of the language in which the examination papers themselves are set, so no language of assessment is asserted here. This site is an independent English-language study resource and is not affiliated with, endorsed by, or connected to the Iraqi Board for Medical Specializations; candidates should confirm the language of their sitting directly with their Scientific Council.

Does this 100-question practice bank simulate clinical cases or replace hospital residency training?

No. The Iraqi Board qualification is an intensive 5-year hospital residency encompassing acute neurology on-call services, stroke thrombolysis, neuro-ICU care, neurophysiology reporting (EEG/EMG), psychiatry rotations, and rigorous bedside long/short cases. This independent 100-question multiple-choice practice bank is strictly a theoretical educational aid designed to test core diagnostic reasoning, pharmacology, neuroanatomy, and guidelines for the Part 1 and Final written papers; it does not simulate OSCE stations or replace accredited clinical training.