Neurology Bootcamp.com

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TABLE OF CONTENTS

Neurology

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.

Embryology Cellular Function Ascending Spinal Cord Tracts Descending Spinal Cord Tracts Brainstem Anatomy Cerebral Cortex Radiculopathy Spinal Cord Syndromes Invasive Spinal Cord Disease Demyelinating Disease Conduction Physiology Neuromuscular Junction (NMJ) Cranial Nerves 1-6 Cranial Nerves 7-12 Vision

TABLE OF CONTENTS

Neurology

16.

Auditory Sensation

17.

Vertigo

18.

Pediatric Brain Tumors

19.

Adult Primary Brain Tumors

20.

Ischemic Cerebrovascular Accidents

21.

Aneurysms and Intracranial Hemorrhage

AfraTafreeh.com 22. Cerebellum and Ventricles 23.

Diencephalon

24.

Basal Ganglia

25.

Neurotransmitter Activity in Psychiatric Disease

26.

Dementia

27.

Headache

28.

Seizures

29.

Traumatic Brain Injuries

AfraTafreeh.com OUTLINE

Neurology: Embryology

1.

Embryology

● ● ● ● ●

A. Notochord B. Neural Tube C. Meninges D. Origins of Nervous Tissue E. Neural Tube Defects

Neurology: Embryology

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• Notochord • Derived from mesoderm • Stimulation of ectoderm à neuroectoderm • ~2.5 weeks gestation AfraTafreeh.com • Neural Tube • Derived from medial ectoderm • Fuses dorsally à neural tube • ~3 weeks gestation

https://commons.wikimedia.org/wiki/File:2912_Neurulation-02.jpg

Neurology: Embryology

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• Epidural Space • Epidural anesthesia • Epidural hematoma • Dura Mater • Derived from mesoderm • Subdural Space • Subdural hematoma • Arachnoid Mater • Derived from neural crest cells • Subarachnoid Space • Contains CSF • Lumbar puncture • Subarachnoid Hemorrhage • Pia Mater • Derived from neural crest cells

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Neurology: Embryology

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Origins of Nervous Tissue Embryologic Origin

Forebrain

Midbrain Hindbrain

Vesicle

High Yield Derivatives

Diencephalon

Hypothalamus Thalamus Pineal gland

AfraTafreeh.com Prosencephalon

Mesencephalon

Telencephalon

Cerebral hemispheres Basal ganglia (not all of it)

Mesencephalon

Midbrain

Metencephalon

Cerebellum Pons

Myelencephalon

Medulla

Rhombencephalon

Neurology: Pathophysiology: Brain

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• Anencephaly • Failure of rostral neuropore closure • Elevated AFP

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Embryologic Cranial Defects Syndrome

Anencephaly

Lissencephaly

Detail

Signs and Symptoms

Absence of forebrain

Fatal, incompatible with life

Lack of cortical sulci and gyri Microcephaly Ventriculomegaly Hydrocephalus Craniofacial abnormalities

Neurology: Pathophysiology: Spinal Cord

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Spinal Defects Syndrome

Detail

Spina Bifida Occulta

Vertebral Defect

Signs and Symptoms Patch of hair AfraTafreeh.com Skin dimple

Meningocele

Meninges through vertebral defect

+/- Motor impairment, developmental delay, bladder and bowel incontinence Myelomeningocele

Spinal cord through vertebral defect

https://commons.wikimedia.org/wiki/File:Typesofspinabifida.jpg

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⚪ A. Failure of closure of the rostral neuropore ⚪ B. Failure of closure of the caudal neuropore ⚪ C. Degeneration of anterior horn cells ⚪ D. Protrusion of meninges through a bony defect ⚪ E. Protrusion of neural tissue through a bony defect

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A 27-year-old female with a past medical history of generalized anxiety disorder and recurring seizures that began during adolescence presents to her obstetrician reporting that she had multiple positive pregnancy tests over the course of the past 18 weeks. She states that she has avoided prenatal care up to this point because she has felt more anxious since she found out she was pregnant. She also states that she has been taking more of her medications to calm her anxiety. When questioned she mentions she is particularly concerned of her higher stress levels precipitating a seizure episode. Her last seizure episode was approximately 4 years prior to this visit. Her vitals are stable. Prenatal and fetal assessments are performed and some of the results are shown below. Which of the following pathologic processes are most consistent with the patient’s lab and imaging results? Urine dipstick negative for protein. Random glucose 108 mg/dL Fetal ultrasound findings are displayed. Amniotic fluid index 44cm (reference range leg)

Brown Sequard

Spinothalamic tract travels superiorly 1-2 levels prior to decussation.

Penetrating Injury (stab wound)

Ipsilateral LMN at level Ipsilateral UMN below level Contralateral pain/temp loss 1-2 below

Posterior

Neurology: Spinal Cord Syndromes

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Distal Spinal Cord Injury Syndrome

Conus Medullaris

Cauda Equina

Level Affected

AfraTafreeh.com T12-L2

Caudal to L2

Distinguishing Features

Acute onset sphincter incontinence Bilateral saddle anesthesia Tends to be less severe pain Mix of UMN and LMN features Gradual onset sphincter incontinence Unilateral saddle anesthesia Tends to be more severe pain Primarily LMN features

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A 36-year-old male is rushed to the emergency room after being found unconscious outside for an undetermined length of time. His temperature is 96F, blood pressure 102/56, heart rate 106 beats per minute, and respiratory rate is 16 breaths per minute. He is saturating 95% on room air. The patient is found to have a bullet entry wound in the left flank proceeding medially with acute angulation in near proximity to the spinal cord. Which of the following features would be least consistent with this presentation?

⚪ A. Loss of all sensation to innervated structures ipsilateral at the level of the lesion ⚪ B. Left-sided hyperreflexia and muscle weakness below the level of the lesion ⚪ C. Left-sided loss of proprioception and vibration sense below the level of the lesion ⚪ D. Right-sided loss of temperature and pain sensation below the level of the lesion ⚪ E. Left-sided pupillary contraction and drooping of the eyelid

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A 36-year-old male is rushed to the emergency room after being found unconscious outside for an undetermined length of time. His temperature is 96F, blood pressure 102/56, heart rate 106 beats per minute, and respiratory rate is 16 breaths per minute. He is saturating 95% on room air. The patient is found to have a bullet entry wound in the left flank proceeding medially with acute angulation in near proximity to the spinal cord. Which of the following features would be least consistent with this presentation?

AfraTafreeh.com ⚪ A. Loss of all sensation to innervated structures ipsilateral at the level of the lesion ⚪ B. Left-sided hyperreflexia and muscle weakness below the level of the lesion ⚪ C. Left-sided loss of proprioception and vibration sense below the level of the lesion ⚪ D. Right-sided loss of temperature and pain sensation below the level of the lesion " E. Left-sided pupillary contraction and drooping of the eyelid

https://commons.wikimedia.org/wiki/File:Brown-Sequard.svg

AfraTafreeh.com OUTLINE

Neurology: Invasive Spinal Cord Disease

1.

Infectious

● ● ● ● ●

A. Tetanospasmin Toxin B. Rabies Virus C. Poliomyelitis D. Varicella Zoster Virus E. Neurosyphilis

2.

Other

●

A. Spinal Muscular Atrophy

Neurology: Invasive Spinal Cord Disease

• Mechanism of Action • Tetanospasmin travels à Renshaw cells in spinal cord • Cleaves SNARE proteinsà ↓ inhibitory neurotransmitter • GABA, Glycine are primaryAfraTafreeh.com inhibitory neurotransmitters • !-motor neurons unregulated • Clinical Signs and Symptoms • Spastic paralysis • Trismus (Lock jaw) • Risus Sardonicus • Opisthotonos • Foul smelling umbilical stump (neonates)

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https://en.wikipedia.org/wiki/Tetanus#/media/File:Neur otransmitter_vesicle_before_and_after_exposure_to_ Tetanus_Toxin.jpg

https://en.wikipedia.org/wiki/Tetanus#/m edia/File:Opisthotonus_in_a_patient_suff ering_from_tetanus__Painting_by_Sir_Charles_Bell__1809.jpg

Neurology: Invasive Spinal Cord Disease

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• Mechanism of Action • Rabies virus binds to nicotinic acetylcholine receptor • Retrograde migration (dynein) à Brainà Encephalitis • Long incubation period • Reservoir • Worldwide: Rabid dogs • U.S.: Bats (also skunks, raccoons, and other animals) • Clinical Signs and Symptoms • Nonspecific overall • Hydrophobia • Photophobia • Paralysis

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Neurology: Invasive Spinal Cord Disease

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• Classic Presentations of Paralytic Poliomyelitis • Unvaccinated child • Classically affects the proximal muscles • Severe muscle pain AfraTafreeh.com • Ascending asymmetric flaccid paralysis (LMN) • Remember your LMN Signs • Fasciculations • Hyporeflexia • Hypotonia • Muscle atrophy Image credit: https://en.wikipedia.org/wiki/Polio#/media/File:Polio_spinal_diagram-en.svg

Neurology: Invasive Spinal Cord Disease

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• Varicella Zoster Virus • • • •

Primary infection à chicken pox Remains dormant in dorsal root ganglia Reactivation à shingles Reactivation classically in immunocompromised patients

• Classic Presentations of Shingles • •

Painful erythematous rash à vesicular Dermatomal distribution, does NOT cross midline

• Variants • •

Herpes Ophthalmicus Herpes Oticus (Ramsay Hunt Syndrome)

• Treatment • •

Acyclovir, Valacyclovir Post-herpetic neuralgia major complication to untreated

https://en.wikipedia.org https://en.wikipedia.org/wiki/Herpes_zoster_ophthalmicus https://en.wikipedia.org/wiki/Shingles#/media/File:Shingles.JPG /wiki/Trigeminal_nerve #/media/File:Trigeminal_herpes_with_uveitis_and_keratitis .jpg

https://en.wikipedia.or g/wiki/Shingles#/medi a/File:Herpes_zoster_ chest.png

Neurology: Invasive Spinal Cord Disease

• Classic Presentations of Neurosyphilis • Immunocompromised patient or poor access to medical care • Possible new onset dementia at an early age • Tabes Dorsalis à broad-based ataxia, positive Romberg AfraTafreeh.com • Loss of proprioception • Areflexia • Argyll Robertson Pupil • Light-near dissociation • Classically associated with neurosyphilis

https://commons.wikimedia.org/wiki/File:Argyll_Robertson_pupil_light_reflex_vs_accommodation_reflex.jpg

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Neurology: Invasive Spinal Cord Disease

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• Classic Presentation of Werdnig-Hoffman Disease (SMA Type I) • Onset between 0-6 months of age, death by 2 years of age • Symmetric flaccid paralysis • Cranial nerves classically spared (normal eye movements) • Lower motor neuron disease • General Information • Autosomal recessive mutation in SMN1 gene, chromosome 5 • Muscle biopsy: Atrophy of motor units

https://commons.wikimedia.org/wiki/File:Polio_spinal_diagram-en.svg

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A researcher is attempting to understand the pathogenesis of the Rabies virus. It is thought that the Rabies virus has interactions with p75 neurotrophin receptors (p75NTR) at peripheral neurons. This interaction has been postulated to allow the virus to enter the neuronal tissue and travel along the axon. It was found that the Rabies virus transport kinetics revealed a preference for transport in p75NTR-dependent compartments when compared to p75NTR-independent compartments. The researcher attempts to study the transport kinetics of the Rabies virus when adding a cell permeable molecular target, TAT-Pep50 in mice. Assuming TATAfraTafreeh.com Pep50 administration demonstrated an overall decrease in mortality in mice infected with rabies virus, which of the following would best explain it’s mechanism of action? ⚪ A. Upregulation of dynein motor proteins along axonal microtubules in the central nervous system ⚪ B. Upregulation of dynein motor proteins along axonal microtubules in the peripheral nervous system ⚪ C. Upregulation of p75NTRs at peripheral nerves ⚪ D. Upregulation of acetylcholine receptors in peripheral nerves ⚪ E. Upregulation of ATPase inhibitors selective to dynein motor proteins at sites of high p75NTR expression ⚪ F. Upregulation of ATPase inhibitors selective to kinesin motor proteins at sites of high p75NTR expression

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A researcher is attempting to understand the pathogenesis of the Rabies virus. It is thought that the Rabies virus has interactions with p75 neurotrophin receptors (p75NTR) at peripheral neurons. This interaction has been postulated to allow the virus to enter the neuronal tissue and travel along the axon. It was found that the Rabies virus transport kinetics revealed a preference for transport in p75NTR-dependent compartments when compared to p75NTR-independent compartments. The researcher attempts to study the transport kinetics of the Rabies virus when adding a cell permeable molecular target, TAT-Pep50 in mice. Assuming TATPep50 administration demonstrated an overall decrease in mortality in mice infected with rabies virus, which of the following would best explain it’s mechanism of action? ⚪ A. Upregulation of dynein motor proteins along axonal microtubules in the central nervous system ⚪ B. Upregulation of dynein motor proteins along axonal microtubules in the peripheral nervous system ⚪ C. Upregulation of p75NTRs at peripheral nerves ⚪ D. Upregulation of acetylcholine receptors in peripheral nerves $ E. Upregulation of ATPase inhibitors selective to dynein motor proteins at sites of high p75NTR expression ⚪ F. Upregulation of ATPase inhibitors selective to kinesin motor proteins at sites of high p75NTR expression

OUTLINE

Neurology: Demyelinating Disease

1.

Demyelinating Disease

● ● ● ● ● ● ●

A. Guillain-Barre Syndrome B. Multiple Sclerosis C. Progressive Multifocal Leukoencephalopathy D. Charcot Marie Tooth Disease E. Metachromatic Leukodystrophy F. Central Pontine Myelinolysis G. Subacute Sclerosing Panencephalitis

2.

Lesions of Vision in Multiple Sclerosis

● ● ●

A. Optic Neuritis B. Marcus Gunn Pupil C. Internuclear Ophthalmoplegia

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Neurology: Demyelinating Disease Neurology: Invasive Spinal Cord Disease

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• Classic Presentations of GBS • • • •

Recent GI infection or URI Ascending symmetric flaccid paralysis (LMN) Campylobacter jejuni is the most important to remember overall Cytomegalovirus is the most common virus

• Cerebrospinal Fluid Differential • • •

Albuminocytological dissociation in both Poliomyelitis and GBS Pleocytosis more classic for Poliomyelitis GBS unlikely with pleocytosis

• Management • •

Plasmapheresis or intravenous immunoglobulins No corticosteroids

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Neurology: Demyelinating Disease Neurology: Invasive Spinal Cord Disease

• Pathophysiology •

Demyelination in CNS, oligodendrocyte axonal degeneration

• Classic Presentation • •

Young patient, classically Caucasian female AfraTafreeh.com Optic Neuritis à Painful, unilateral

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Neurology: Demyelinating Disease Neurology: Invasive Spinal Cord Disease

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• Pathophysiology •

Demyelination in CNS, oligodendrocyte axonal degeneration

• Classic Presentation • • •

Young patient, classically Caucasian female Optic Neuritis à Painful, unilateral Marcus Gunn Pupil (relative afferent pupillary defect)

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Neurology: Demyelinating Disease Neurology: Invasive Spinal Cord Disease

• Pathophysiology •

Demyelination in CNS, oligodendrocyte axonal degeneration

• Classic Presentation • • • •

Young patient, classically Caucasian female AfraTafreeh.com Optic Neuritis à painful, unilateral Marcus Gunn Pupil (relative afferent pupillary defect) Unilateral/Bilateral Internuclear Ophthalmolpegia (lesion to MLF)

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Neurology: Demyelinating Disease Neurology: Invasive Spinal Cord Disease

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• Pathophysiology •

Demyelination in CNS, oligodendrocyte axonal degeneration

• Classic Presentation • • • • • • • •

Young patient, classically Caucasian female Optic Neuritis à painful, unilateral Marcus Gunn Pupil (relative afferent pupillary defect) Bilateral Internuclear Ophthalmolpegia (lesion to MLF, heavily myelinated) Uhthoff phenomenon Bladder or bowel incontinence Lhermitte's sign Upper motor neuron signs

Neurology: Demyelinating Disease Neurology: Invasive Spinal Cord Disease

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• Imaging: MRI • •

Periventricular white matter lesions Dawson’s fingers

• Lumbar Puncture • •

AfraTafreeh.com Oligoclonal bands ↑ WBC, predominantly lymphocytes

• Management • • •

Acute setting consider high dose steroids Interferon-! Natalizumab à increased risk of progression to PML

https://radiopaedia.org/cases /multiple-sclerosis-dawsonsfingers-3

Neurology: Demyelinating Disease Neurology: Invasive Spinal Cord Disease

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• Pathophysiology • •

Reactivation of JC virus, typically in immunocompromised host Oligodendrocyte destruction à demyelination

• Classic Presentations of PML • •

Poorly controlled HIV history or recent treatment with natalizumab Unusual behavioral changes +/- focal neurologic deficits

• Diagnostics • •

Widespread non-enhancing white matter lesions JC Virus PCR in CSF https://en.wikipedia.org/wik i/Progressive_multifocal_le ukoencephalopathy

https://radiopaedia.org/ar ticles/progressivemultifocalleukoencephalopathy?lan g=us

Neurology: Demyelinating Disease Neurology: Invasive Spinal Cord Disease

• Charcot-Marie-Tooth Disease • • • •

Triad: Hammer toe, pes cavus, foot drop Distal, symmetric, sensory and motor neuropathy PNS Lower motor neuron signs

AfraTafreeh.com • Metachromatic Leukodystrophy • • • •

Autosomal recessive, deficiency of arylsulfatase A Build up of cerebroside sulfate leading to demyelination CNS and PNS Motor skill development regress in infants and young children

• Central Pontine Myelinolysis • •

Rapid sodium correction “Locked in” Syndrome (similar to pontine basilar infarction)

• Subacute Sclerosing Panencephalitis •

History of persistent measles infection

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A 28-year-old fully vaccinated male with no significant past medical history presents to an urgent care clinic for abdominal cramping and watery ⚪ A. Apoptosis of ventral horn cells diarrhea. He is given a short course of antibiotics and his diarrhea ⚪ B. Molecular mimicry and destruction to Schwann cells resolves. Three weeks later he presents to the emergency room after a ⚪ C. Molecular mimicry and destruction to oligodendrocytes ⚪ D. Replication and reactivation of virus in dorsal root ganglia fall episode. He states he was attempting to walk on the treadmill at his ⚪ E. Inhibition of glycine release via SNARE proteins local fitness center when he lost his balance and fell backward. He states that over the past week he has had difficulty climbing the stairs and thought it was because he was sleeping awkwardly on his legs. Muscle strength testing is 3/5 bilaterally at the lower extremities and reflexes are absent at S1 bilaterally. A lumbar puncture is performed with findings shown below. Which of the following is most consistent with the pathologic mechanism likely causing this patient’s current presentation? Opening Pressure: 10cm H2O Appearance: Clear White Blood Cells: 3 cell/uL (reference range: 0-5 cells/uL) Protein: 722 mg/L (reference range: BC, Right BC > AC, lateralization to the right ⚪ B. Left AC > BC, Right AC > BC, lateralization to the left ⚪ C. Left BC > AC, Right AC > BC, lateralization to the left ⚪ D. Left AC > BC, Right AC > BC, lateralization to the right ⚪ E. Left AC > BC, Right AC > BC, no lateralization

Legend: Air conduction: AC Bone conduction: BC

https://commons.wikimedia.org/wiki/File:Cholesteatom_kuppelraum_1a.jpg

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A 24-year-old male presents to his family medicine physician for foulsmelling drainage from the left ear. He also states that he has experienced worsening hearing loss from his left side for the past year. He states that he works as a librarian and rarely listens to music. He denies any loss of sensation on the face or fever. A fundoscopic exam is performed revealing a gray-brown irregularly shaped mass with dark discoloration to the surrounding epithelia. Scant amounts of discharge are noted.

AfraTafreeh.com Which of the following results of the Weber and Rinne test would be most consistent with the finding in this patient?

⚪ A. Left AC > BC, Right BC > AC, lateralization to the right ⚪ B. Left AC > BC, Right AC > BC, lateralization to the left $ C. Left BC > AC, Right AC > BC, lateralization to the left ⚪ D. Left AC > BC, Right AC > BC, lateralization to the right ⚪ E. Left AC > BC, Right AC > BC, no lateralization

Legend: Air conduction: AC Bone conduction: BC

https://commons.wikimedia.org/wiki/File:Cholesteatom_kuppelraum_1a.jpg

AfraTafreeh.com OUTLINE

Neurology: Vertigo

1.

Fundamental Concepts

● ●

A. Vestibular System Anatomy B. Peripheral vs Central Vertigo

2.

Peripheral Vertigo

● ● ●

A. Benign Paroxysmal Positional Vertigo B. Vestibular Neuritis, Labyrinthitis C. Meniere’s Disease, Acoustic Neuroma

3.

Central Vertigo

● ● ● ●

A. Cerebellar Infarction B. Brainstem Lesions C. Brain Tumor (Posterior Fossa) D. Multiple Sclerosis

Neurology: Vertigo

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• Vestibular System • • •

Semicircular canals: detect angular acceleration in 3 planes Saccule: detect linear motion in vertical plane Utricle: detect linear motion in horizontal plane

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Neurology: Vertigo

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• Peripheral Vertigo • • • •

Lesion à inner ear or vestibulocochlear nerve Vertigo ceases or improves with visual fixation Positional Motor, gait, coordination generally intact

• Central Vertigo • • • •

Lesion à Cerebellum, brainstem nuclei Vertigo does not cease with visual fixation Non-positional, generally continuous Motor, gait, coordination impairment may be present

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Vertigo Peripheral

Central

Neurology: Vertigo

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Peripheral • Pathophysiology: •

Dislodged endolymphatic debris (otoconia) à disrupted semicircular canal function

• Presentation: • • •

Paroxysmal à sudden onset, lasting less than 1 minute AfraTafreeh.com Positional à precipitated by specific head movements Nystagmus

• Diagnostics and Management: • •

Clinical diagnosis Dix-Hallpike maneuver à if + test à Epley maneuver

Neurology: Vertigo

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• Pathophysiology: •

Inflammatory reaction of vestibular nerve

• Presentation: • • • • •

Persistent à degree of vertigo present continuously Positional à precipitated by specific head movements Previous viral URI or otitis media Nystagmus Labyrinthitis: Similar presentation + hearing loss, possibly tinnitus

• Diagnostics and Management: •

Clinical diagnosis

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Peripheral

Neurology: Vertigo

• Pathophysiology: •

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Peripheral

Impaired resorption of endolymph à ↑ volume of endolymph

• Presentation: • • • • • •

Episodic, no trigger (usually) lasts for minutes to hours Unilateral (usually) AfraTafreeh.com Tinnitus Sensorineural hearing loss (normal Rinne test, lateralization of Weber test to unaffected) Nystagmus Acoustic Neuroma: Similar presentation, but not episodic

• Diagnostics and Management: • • •

Acute attack à Vestibular suppressants (meclizine) Secondary prevention à Low sodium diet, avoid triggers Chronic management (refractory) à Thiazide diuretics

Neurology: Vertigo

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• Cerebellar Infarction: • Brain tumor (posterior fossa): • •

Adults: Ependymoma, meningioma, metastatic disease Children: Medulloblastomas

• Central Nervous System Demyelinating Disease: • •

Multiple sclerosis Progressive multifocal leukoencephalopathy

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Central

Neurology: Vertigo

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Peripheral Vertigo Disease

Pathophysiology

Presentation

Diagnostics

Management

Benign paroxysmal positional vertigo

Dislodged otoconia, semicircular canals

Men Vitamin A

Management: • • •

MRI à Generally unremarkable LP à ↑ opening pressure, diagnostic and therapeutic Acetazolamide: Carbonic anhydrase inhibitor

Neurology: Headache

•

Presentation: • • • •

•

Older patient (55-70 years of age) Unilateral, severe, sudden onset, “shooting or stabbing”, “electric shock” pain V2 and V3 distributions classically affected Duration: Several seconds, recurring many times throughout the day

Triggers: •

•

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Talking, chewing, touch

Management: • •

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MRI à Generally unremarkable Carbamazepine: Inactivation of depolarizing Na+ channels

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Neurology: Headache

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High Yield Headache Disease Process

Classic Presentation

Duration

Neurologic Symptoms

Key Associations

Acute Management

Preventative/Chronic Management

Tension Headache

Band-like Bilateral “Achy”, “tight”, or “dull” “Vice-like” headache

Variable

None, no aura

n/a

NSAIDs and/or conservative

Avoid precipitating factors

Migraine

“Throbbing, pulsating” Unilateral Nausea

4-72 hours

+/- Aura Photophobia

Women Genetic predisposition

Sumatriptan Ergotamine

β-blocker TCA Topiramate (low yield)

Cluster Headache

”Sharp” unilateral, periorbital Repeating in “clusters” Cyclical association between attacks (similar times daily)

Age (55*-70)

n/a to Step 1

Carbamazepine

Keep in mind: Test writers may use adjectives such as “sharp” to describe a migraine headache in a question stem. Classic descriptions are not pathognomonic.

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A 34-year-old female with a past medical history of generalized anxiety disorder presents to the emergency department for a headache that has been ongoing for the past 2 hours. The patient reports that she was in a meeting at her office when she suddenly saw “stars” and felt her left arm go numb. She initially thought she may be having a stroke, however her symptoms resolved within five minutes. Shortly thereafter she developed a left-sided 8/10 throbbing headache. She has been unable to eat due to significant nausea. She requests that the lights remain dimmed in the room. Her grandmother has a history of recurrent headaches with no other significant family history. Oral contraceptives are the only prescribed medication that she is currently taking. Vital signs and fundoscopy are shown below. Physical examination is unremarkable. Temperature: 98F (36.7C) Blood Pressure: 130/62 Heart Rate: 104/min Respiratory Rate: 12/min Oxygen Saturation: 100% on room air

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Non-contrast head CT is unremarkable. A serotonin agonist is prescribed to acutely manage the severity of this patient’s headache. Which mechanism of action is most likely consistent with the medication prescribed? ⚪ A. ⚪ B. ⚪ C. ⚪ D. ⚪ E.

Inhibition of enzymatic carbonic anhydrase Binding to inactive voltage-gated sodium channels in cortical tissue Inhibition of calcitonin gene-related peptide release from trigeminal afferent neurons Stimulation of trigeminal afferent neuronal fibers to release substance P Intracranial vessel vasodilation secondary to binding of target receptors on smooth muscle tissue

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A 34-year-old female with a past medical history of generalized anxiety disorder presents to the emergency department for a headache that has been ongoing for the past 2 hours. The patient reports that she was in a meeting at her office when she suddenly saw “stars” and felt her left arm go numb. She initially thought she may be having a stroke, however her symptoms resolved within five minutes. Shortly thereafter she developed a left-sided 8/10 throbbing headache. She has been unable to eat due to significant nausea. She requests that the lights remain dimmed in the room. Her grandmother has a history of recurrent headaches with no other significant family history. Oral contraceptives are the only prescribed medication that she is currently taking. Vital signs and fundoscopy are shown below. Physical examination is unremarkable. Temperature: 98F (36.7C) Blood Pressure: 130/62 Heart Rate: 104/min Respiratory Rate: 12/min Oxygen Saturation: 100% on room air

Non-contrast head CT is unremarkable. A serotonin agonist is prescribed to acutely manage the severity of this patient’s headache. Which mechanism of action is most likely consistent with the medication prescribed? ⚪ A. ⚪ B. $ C. ⚪ D. ⚪ E.

Inhibition of enzymatic carbonic anhydrase Binding to inactive voltage-gated sodium channels in cortical tissue Inhibition of calcitonin gene-related peptide release from trigeminal afferent neurons Stimulation of trigeminal afferent neuronal fibers to release substance P Intracranial vessel vasodilation secondary to binding of target receptors on smooth muscle tissue

OUTLINE

Neurology: Seizures

1.

Overview

● ● ● ●

A. Classification B. Epilepsy C. General Terms D. Triggers and Inciting Causes

2.

Focal Seizure

● ●

A. Focal Aware B. Focal Impaired Awareness

3.

Generalized Onset Seizure

● ● ● ● ●

A. Absence B. Tonic-Clonic C. Myoclonic D. Atonic E. Simple Febrile

AfraTafreeh.com 4.

Status Epilepticus

● ●

A. Definition B. Management

5.

Antiepileptic Medications

● ● ●

A. Narrow Spectrum B. Broad Spectrum C. Other/Varied

Neurology: Seizure

•

Seizure Classification: • • •

•

Ictal: Occurring during the time of seizure Post-ictal: Occurring after the time of seizure

Triggers à Reflex: • • •

•

≥2 unprovoked separated by >24 hours 1 seizure with high risk for subsequent seizure

General Terms: • •

•

Unprovoked: No clear etiology Reflex: Trigger that predisposes to seizure risk (↓ seizure threshold) Provoked: Concurrent with systemic illness or central nervous system pathology

Epilepsy: • •

•

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Flashing lights High fever (infants and young children) Lack of sleep

Inciting Causes à Provoked: • • •

Cerebrovascular accident Traumatic brain injury Electrolyte imbalance

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Neurology: Seizure

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Temporal: Auditory hallucinations

Awareness and consciousness remains intact No post-ictal state

Focal Impaired Awareness (Complex Partial): • • • •

•

Single hemisphere (à +/- global generalization) Localized symptoms at onset

Focal Aware (Simple Partial): • •

•

Frontal: Jerking movement of contralateral extremity

Origin: • •

•

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Awareness impaired, ”blank stare” AfraTafreeh.com Post-ictal state (common) à Todd paralysis Automatisms Common origin à Temporal lobe

Etiology: •

#1 Focal cerebral lesion

Parietal: Numbness of contralateral extremity Occipital: Visual hallucinations

Jacksonian March: Spread of abnormal electrical activity to nearby areas of the motor cortex

Focal Seizure Presentation à Contralateral Face or Limb Automatisms Myoclonus Tonic and/or clonic Contractions Sensory disturbances Behavioral changes

Neurology: Seizure

• •

•

•

•

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Origin: • Global generalization • Generalized symptoms at onset Absence: • Loss of consciousness, “blank stare” for short intervals (~ 5-15 seconds) • Generally, no post-ictal state, consciousness returns immediately following ictal-state • Child or adolescent • EEG à 3-Hz spike-wave complex • First-line Rx: Ethosuximide Tonic-Clonic (grand mal): • Loss of consciousness • Post-ictal state (common) • Bilateral muscle contractions (tonic) and rhythmic twitching (clonic) • “Eyes rotate to the back of the head” • Lateral tongue lacerations • Urinary or stool incontinence • First-line Rx: Broad-spectrum AEDs (e.g., Levetiracetam) Myoclonic: • Nonrhythmic jerking movements • No loss of consciousness, no post-ictal state Atonic: • “Drop seizure” • Acute onset diffuse loss of muscle tone

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Neurology: Seizure

•

Pathophysiology: •

•

Significant fever (>104F) 6 months to 5 years of age Simple Febrile Seizure: Brief generalized, nonrecurring seizure Complex Febrile Seizure: Long lasting focal at onset, recurring seizure

Associations: • •

•

Hyperthermia à ↑ CSF cytokines/interleukins

Presentation: • • • •

•

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Viral infection: Classic cause = Roseola à HHV-6 Genetic predisposition

Management: • •

Simple febrile seizure: Conservative NSAIDs, acetaminophen à ↓ PGE2 à ↓ Central hypothalamic temperature setpoint

Neurology: Seizure

•

Definition: • •

•

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Single seizure, ≥5 minutes Multiple seizures, incomplete level of consciousness regained between each episode

Management: • •

Abort seizure: Intravenous benzodiazepines à positive allosteric modulator à hyperpolarizing Prevention of recurrence: Intravenous phenytoin

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Neurology: Seizure

Bootcamp.com https://commons.wikimedia.org/wiki/File:Gingivitis_(crop).jpg

• • • • •

Valproate: Adverse effects: Neural tube defects Levetiracetam: Binds SV2A à modulation of glutamate and GABA release Lamotrigine: Adverse effects: Stevens-Johnson syndrome

Broad

Fetal Hydantoin Syndrome Fingernail hypoplasia Excess hair production Intrauterine growth restriction

Phenytoin: • MOA: Inhibition of pre-synaptic voltage-gated sodium channels • Adverse effects: Teratogenic, gingival hyperplasia, hirsutism • Cytochrome P450 inducer, zero order elimination Carbamazepine: • Primary use: Focal seizures and trigeminal neuralgia • MOA: Inhibition of pre-synaptic voltage-gated sodium channels • Cytochrome P450 inducer (strong) • Adverse effects: SJS, Aplastic anemia, teratogenic Gabapentin: Inhibition of pre-synaptic voltage-gated calcium channels Ethosuximide: Inhibition of voltage-gated T-type calcium channels in thalamus

Narrow

•

•

Phenobarbital: • Primary use: Neonatal seizure • MOA: GABA-A agonist, ↑ duration of chloride channel opening • Cytochrome P450 inducer Lorazepam: • Primary use: Abort acute seizure activity and status epilepticus • MOA: GABA-A agonist, ↑ frequency of chloride channel opening

•

Other

•

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A 6-year-old female with no significant past medical history is seen by her pediatrician for worsening academic performance. Her father is convinced that she has attention deficit disorder. He references three occasions of which he was contacted by his daughter’s teacher to inform him of her “day-dreaming”. He also states that she stares off into the distance when playing with her friends outside. The patient has no history of missed milestones and height, and weight are within the appropriate reference ranges for her age. Her temperature is 98F (36.7C) with otherwise unremarkable vital signs. On physical examination no focal neurologic deficits are appreciated. Tongue lacerations are absent. Electroencephalography is performed in the setting of hyperventilation. The results are shown below. A medication is prescribed by her pediatrician.

Which mechanism of action is most likely consistent with the medication prescribed? ⚪ A. ⚪ B. ⚪ C. ⚪ D. ⚪ E. ⚪ F.

Reversible inhibition of cyclooxygenase-1 enzymes Increase in frequency of chloride channel opening Increase in duration of chloride channel opening Inhibition of inactivated sodium channels Selective norepinephrine reuptake inhibitor Inhibition of thalamic T-type calcium channels

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A 6-year-old female with no significant past medical history is seen by her pediatrician for worsening academic performance. Her father is convinced that she has attention deficit disorder. He references three occasions of which he was contacted by his daughter’s teacher to inform him of her “day-dreaming”. He also states that she stares off into the distance when playing with her friends outside. The patient has no history of missed milestones and height, and weight are within the appropriate reference ranges for her age. Her temperature is 98F (36.7C) with otherwise unremarkable vital signs. On physical examination no focal neurologic deficits are appreciated. Tongue lacerations are absent. Electroencephalography is performed in the setting of hyperventilation. The results are shown below. A medication is prescribed by her pediatrician.

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Which mechanism of action is most likely consistent with the medication prescribed? ⚪ A. ⚪ B. ⚪ C. ⚪ D. ⚪ E. $ F.

Reversible inhibition of cyclooxygenase-1 enzymes Increase in frequency of chloride channel opening Increase in duration of chloride channel opening Inhibition of inactivated sodium channels Selective norepinephrine reuptake inhibitor Inhibition of thalamic T-type calcium channels

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https://commons.wikimedia.org/wiki/File:Spike-waves.png

AfraTafreeh.com OUTLINE

Neurology: Traumatic Brain Injury and Herniation

1.

Diffuse Axonal Injury

● ● ● ●

A. Etiology B. Pathophysiology C. Histopathology D. Imaging

2.

Intracranial Hypertension

● ● ● ● ●

A. Classic Etiologies B. Cushing Reflex C. Signs of Increased Intracranial Pressure D. Imaging Findings E. Management

3.

Brain Herniation

● ● ●

A. Uncal (Transtentorial) Herniation B. Subfalcine (Cingulate) Herniation C. Tonsillar Herniation

4.

Decerebrate vs Decorticate Posturing

● ● ●

A. Decerebrate Posturing B. Decorticate Posturing C. Absence of Motor Tone

Neurology: Traumatic Brain Injury and Herniation

Bootcamp.com https://commons.wikimedia.org/wiki/File:Diffuse_axonal_injury-_cMRT_nach_3_Tagen.jpg https://commons.wikimedia.org/wiki/File:Contrecoup.svg

•

Etiology: • • •

•

Widespread shearing of white matter tracts

Histopathology: • •

•

Coup-contrecoup injury, extreme rotational acceleration/deceleration forces Motor vehicle accidents Penetrating and blast trauma

Pathophysiology: •

•

Initial diagnostics in TBIà Head CT

Axonal bulb formation (diffuse axonal edema) AfraTafreeh.com Accumulation of axonal transport proteins

Imaging: • •

Head CT scan: Generally unremarkable Brain MRI: Diffuse punctate hemorrhages at the site of the gray-white matter junction and corpus callosum

Neurology: Traumatic Brain Injury and Herniation

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CPP = MAP - ICP •

•

•

•

•

Classic Etiologies: • Mass lesion (brain tumor, aneurysm, hematoma) • Idiopathic intracranial hypertension • Hydrocephalus • Intracranial hemorrhage Cushing Reflex: • Hypertension (↑ MAP) • Bradycardia • Irregular respirations à Respiratory depression Signs of ↑ Intracranial Pressure • Bilateral papilledema • Lateral rectus palsy • Ipsilateral fixed, dilated pupil, “down and out” eye +/- ptosis • Bulging fontanelle (infants) Imaging Findings: • Active hemorrhage, midline shift • Ventriculomegaly Management: • Hyperventilation (↓PaCO2 à vasoconstriction à ↓ cerebral blood volume) • Elevate head of the bed • Intravenous mannitol

Neurology: Traumatic Brain Injury and Herniation

Bootcamp.com https://commons.wikimedia.org/wiki/File:Brain_herniation_types-2.svg

•

Uncal (Transtentorial) Herniation: • • • •

•

Subfalcine (Cingulate) Herniation: • • •

•

Medial temporal lobe beneath tentorium cerebelli Initial Sign: Ipsilateral fixed, dilated pupil (CN III) à “down and out” positioning +/- ptosis Ipsilateral and/or contralateral weakness (cerebral peduncle) Contralateral homonymous hemianopia with macular sparing or blindness (PCA) Cingulate gyrus under falx cerebri Contralateral lower extremity weakness (ACA territory) AfraTafreeh.com Obstructive hydrocephalus (foramen of Monro)

Tonsillar Herniation: • •

Classic Cause: Chiari malformations Obstructive hydrocephalus (cerebral aqueduct)

Neurology: Traumatic Brain Injury and Herniation

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Bootcamp.com https://commons.wikimedia.org/wiki/File:Decorticate.PNG https://commons.wikimedia.org/wiki/File:Decerebrate.jpg

•

Decorticate (Flexor) Posture: • •

•

Decerebrate (Extensor) Posture: • •

•

Lesion to neural tissue above the red nucleus ↑ neuronal activity to the upper limb flexors (Flexors > Extensors) Lesion to neural tissue below the red nucleus ↓ neuronal activity to the upper limb flexors (Flexors < Extensors)

Absence of Motor Tone: •

Classic Cause: Cervical spinal cord injury

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A 67-year-old female is brought to the emergency department by paramedics following acute onset right-sided lower extremity weakness and numbness. The patient has a past medical history of chronic hypertension, iatrogenic hypothyroidism, and atrial fibrillation. A list of medications is provided by the patient’s spouse including lisinopril, levothyroxine, and rivaroxaban. The patient’s spouse states that she was in her usual state of health this morning but has become increasingly confused en route to the hospital. Vitals signs are shown below. An emergent non-contrast CT of the head is performed and shown. An immediate neurosurgical consultation is placed. Temperature: 99.0 F (37.2 C) Blood pressure: 170/68 mmHg Heart rate: 58/min Respirations: 10/min Oxygen saturation: 99% on room air Glasgow coma scale: 12

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Which of the following best explains the cause of neurologic deficit in this patient? ⚪ A. ⚪ B. ⚪ C. ⚪ D. ⚪ E.

Widespread cerebral hypoperfusion Hemispheric herniation inferior to the falx cerebri Diffuse shearing of white matter tracts Localized shearing of cortical bridging veins Acute high-impact fracture to the left pterion

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A 67-year-old female is brought to the emergency department by paramedics following acute onset right-sided lower extremity weakness and numbness. The patient has a past medical history of chronic hypertension, iatrogenic hypothyroidism, and atrial fibrillation. A list of medications is provided by the patient’s spouse including lisinopril, levothyroxine, and rivaroxaban. The patient’s spouse states that she was in her usual state of health this morning but has become increasingly confused en route to the hospital. Vitals signs are shown below. An emergent non-contrast CT of the head is performed and shown. An immediate neurosurgical consultation is placed. Temperature: 99.0 F (37.2 C) Blood pressure: 170/68 mmHg Heart rate: 58/min Respirations: 10/min Oxygen saturation: 99% on room air Glasgow coma scale: 12 Which of the following best explains the cause of neurologic deficit in this patient? ⚪ A. $ B. ⚪ C. ⚪ D. ⚪ E.

Widespread cerebral hypoperfusion Hemispheric herniation inferior to the falx cerebri Diffuse shearing of white matter tracts Localized shearing of cortical bridging veins Acute high-impact fracture to the left pterion

Bootcamp.com https://commons.wikimedia.org/wiki/File:Subfalcine-herniation-001.jpg