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Neurology Flashcards

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USMLE® Step 1 flashcards
1
Q

Name the 3 primary, and five secondary vesicles of the developing adult brain:

A

Forebrain (prosencephalon) becomes the telencephalon and diencephalon. Midbrain (mesencephalon) persists as the mesencephalon. Hindbrain (rhombencephalon) becomes the metencephalon and the myelencephalon.

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2
Q

Name the derivatives of the 5 secondary vesicles of the developing brain:

A

Telencephalon becomes cerebral hemispheres and lateral ventricles. Diencephalon becomes the thalamus and third ventricle. Mesencephalon becomes the midbrain and aqueduct. Metencephalon becomes the pons, cerebellum, and upper part of the 4th ventricle. Myelencephalon becomes the medulla and lower part of the 4th ventricle.

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3
Q

Neuropores are supposed to fuse when? Which two biochemical markers can help predict this?

A

4th week of gestation. Amniotic AFP and AChE and maternal AFP. Unless it is SPO (normal AFP).

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4
Q

Hemispheres separate when? Failure to separate is associated with what? Characteristic MRI findings of failure to fuse?

A

Usually between the 5th and 6th week. Seen in Trisomy 21 and FAS. MRI shows mono ventricle and fusion of basal ganglia.

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5
Q

How do you distinguish Chiari I from Chiari II malformations?

A

Chiari I involves one structure; the cerebellar tonsils. cf Chiari II which also involves the vermis. Chiari I is associated with spinal cavitations. Chiari II is associated with lumbosacral myelinmeningocoele and causes hydrocephalus.

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6
Q

What is Dandy Walker syndrome?

A

Agenesis of the cerebellar vermis with cystic enlargement of the 4th ventricle. Presents with enlarged posterior fossa and cerebellar signs. Associated with non-communicating hydrocephalus, and spina bifida.

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7
Q

Schwann cells versus Oligodendrocytes: Number of axons myelinated? Injured in which diseases?

A

Schwann cells are located in the PNS and only myelinated one axon. They may be injured in GBS. Oligodendrocytes myelinate many axons (~30) in the CNS and may be injured in MS, PML, and the leukodystrophies.

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8
Q

Merkel discs: Have what type of fibres? Are responsible for what senses? Are located where?

A

Large, myelinated fibres. Responsible for pressure, deep touch, position sense. Located in the finger tips and superficial skin.

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9
Q

Describe the implication and histological appearance of Chromatolysis.

A

Reaction of neuronal cell body to axonal injury. Changes reflect increased protein synthesis. Histological appearances of round cellular swelling, displacement of the nucleus to the periphery, and dispersion of Nissl substance throughout the cytoplasm.

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10
Q

What is Nissl substance?

A

Nissl substance or a Nissl body is a large granular body found in neurons. These granules are of rough endoplasmic reticulum (RER) with rosettes of free ribosomes, and are the site of protein synthesis.

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11
Q

What is the location of synthesis of:

Ach

Dopamine

GABA

Norepinephrine

Serotonin

A

Ach - Basal nucleus of Meynert

Dopamine - Ventral tegmenjtum and SNc

GABA - Nucleus accumbens

Norepinephrine - Locus ceruleus

Serotonin - Raphe nucleus

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12
Q

What are the roles of the Hypothalamus?

A

(TANHATS) Thirst. Regulates adenohypophysis and neurohypophysis. Controls Hunger, Autonomic nervous system, Temperature, and Sexual urges.

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13
Q

What are the anatomical divisions of the hypothalamus? What are their functions?

A

Lateral area - Hunger (+ghrelin, -leptin)

Ventromedial area - Satiety (+leptin)

Anterior - Cooling, parasympathetic

Posterior - Heating, sympathetic

Suprachiasmatic nucleus - Circadian rhythm

Supraoptic and paraventricular nuclei - ADH and Oxytocin

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14
Q

What are the stages of sleep, their make-up of total sleep, and the EEG wave forms associated with each?

A

Awake eyes open - Beta waves (highest freq, low amp)

Awake eyes closed - Alpha waves

N1 (5%) Light sleep; Theta waves

N2 (45%) Deeper sleep; Sleep spindles and K complexes

N3 (25%) Deepest non-REM; Delta (lowest freq, highest amp)

REM (25%) Loss of tone etc. Beta waves (at night, BATS Drink Blood)

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15
Q

What is the role of the Thalamus?

A

The Thalamus is the major relay for ascending sensory information except olfaction.

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16
Q

Which part of the thalamus relays and coordinates: Vibration, Pain, Pressure, Proprioception, Light touch, and Temperature? What is the relay destination?

A

The ventral posterolateral nucleus. The primary somatosensory cortex.

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17
Q

Which part of the thalamus relays and coordinates: Face sensation and taste? What is the relay destination?

A

The ventral posteromedial nucleus. The primary somatosensory cortex.

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18
Q

Which part of the thalamus relays and coordinates: Vison? What is the relay destination?

A

The lateral geniculate nucleus. The calcarine sulcus.

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19
Q

Which part of the thalamus relays and coordinates: Hearing? What is the relay destination?

A

The medial geniculate nucleus. The auditory cortex of the temporal lobe.

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20
Q

Which part of the thalamus relays and coordinates: Motor function? What is the relay destination?

A

The ventral lateral nucleus. The motor cortex.

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21
Q

What structures comprise the Limbic system? What is their role?

A

Hippocampus, Mamillary bodies, Anterior thalamic nuclei, cingulate gyrus, entorhinal cortex. Responsible for feeding, fighting, fleeing, feeling, sex.

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22
Q

What are the 4 Dopaminergic pathways in the brain? What does altering their activity cause symptomatically?

A

Mesocortical - Reduced activity = “Negative” symptoms Mesolimbic - Increased activity = “Positive” symptoms **Nigrostriatal - Reduced activity = Parkinsonism Tuberoinfundibular - Reduced activity = Increased PrL, reduced libido etc.

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23
Q

What are the 4 anatomical components of the Basal Ganglia?

A

Striatum

Pallidum

SN pars compacta

Subthalamic nuclei

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24
Q

Describe the input/output pathways of the basal ganglia and how they relate to Parkinson’s disease.

A
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25
Q

Describe the relationship of CPP to changes in oxygen versus carbon dioxide.

A

Hypoxaemia increases CPP only when PO2 <50mmHg

whereas

CPP is directly proportional to PCO2 until PCO2 >90

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26
Q

Which cranial nerves emerge from:

Above the pons?

In the pons?

In the medulla?

Which cranial nerves emerge medially?

A

4 CN from above the pons - I, II, III, IV

4 CN from in the pons - V, VI, VII, VIII

4 CN from in the medulla - IX, X, XI, XII

4 CN emerge medially - III, IV, VI, XII

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27
Q

Where do the cranial nerve nuclei arise?

A

2 from midbrain - III, IV

4 from pons - V, VI, VII, VIII

3 from medulla - IX, X, XII

1 from spinal cord - XI

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28
Q

What is the role of:

The pineal gland?

The superior colliculi?

The inferior colliculi?

A

Pineal gland - melatonin secretion, circadian rhythm

Superior colliculi - Conjugate vertical gaze

Inferior colliculi - Auditory signal relay

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29
Q

What is the role of the Nucleus Solitarius?

Which cranial nerves originate here?

A

Visceral sensory information - taste, baroreceptors, gut distension

CN VII, IX, X

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30
Q

What is the role of the Nucleus Ambiguus?

Which cranial nerve nuclei arise from here?

A

Motor innervation of the pharynx, larynx, upper oesophagus (eg. swallowing, palate elevation)

CN IX, X, XI

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31
Q

Where in the spinal cord do the following nerve fibres ascend/descend?

Pressure, Vibration, Fine Touch, Proprioception?

Pain and Temperature?

Crude touch and pressue?

Voluntary motor?

A

Pressure, Vibration, Fine Touch, Proprioception - Dorsal column

Pain and Temperature - Lateral Spinothalamic Tract

Crude touch and pressue - Anterior Spinothalamic Tract

Voluntary motor - Anterior and Lateral Corticospinal Tract

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32
Q

What is internuclear ophthalmoplegia?

Where is the lesion?

In what disease typically?

A

Impaired aDDuction of ipsilateral eye, nystagmus of contralateral eye with ABduction

(normal eye is rapidly trying to reset the gaze center for the abnormal eye)

Medial longitudinal fasciculus.

MS.

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33
Q

What is Wernicke-Korsakoff syndrome?

Where is the lesion?

What is the typical pathology?

A

Confusion, Ataxia, Nystagmus, Ophthalmoplegia

Mamillary bodies

Alcoholism

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34
Q

What is Kluver-Bucy syndrome?

Where is the lesion?

What typically causes it?

A

Disinhibited behaviour; hypersexuality, hyperphagia, hyperorality.

Amygdala

HSV-1 Encephalitis.

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35
Q

What is Parinaud syndrome?

Where is the lesion?

What is the typical cause?

A

Paralysis of conjugate vertical gaze

Superior colliculus

Pinealoma, hydrocephalus, stroke.

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36
Q

Stoke Pattern:

Contralateral paralysis and sensory loss - face and upper limb

Aphasia if in dominant, hemineglect if in non-dominant

A

Middle Cerebral Artery

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37
Q

Stroke Pattern:

Contralateral paralysis and sensory loss - lower limb

A

Anterior cerebral artery.

38
Q

Stroke Pattern:

Contralateral paralysis and/or sensory loss - face and body

Absence of cortical signs (eg. neglect, aphasia, VF loss)

A

Lenticulo-striate artery

(unmanaged HTN)

39
Q

Stroke Pattern:

Contralateral paralysis - upper and lower limbs

Reduced contralateral proprioception

Ipsilateral hypoglossal dysfunction

A

Anterior spinal artery.

(Medial Medullary Syndrome)

40
Q

Stroke Pattern:

Dysphagia, hoarseness, reduced gag reflex.

Vomiting, vertigo, nystagmus.

Reduced pain and temperature on contralateral body but ipsilateral face.

Ipsilateral Horner’s. Ataxia, dysmetria.

A

Lateral medullary syndrome.

Wallenburg syndrome.

Posterior inferior cerebellar artery.

41
Q

Stroke Pattern:

Paralysis of face, reduced lacrimation, salivation, and taste.

Vomiting, vertigo, nystagmus.

Reduced pain and temperature sensation on contralateral body, ipsilateral face.

Ipsilateral Horner’s. Ataxia, dysmetria.

A

Lateral Pontine syndrome.

Anterior inferior cerebellar artery.

“Facial droop means AICAs pooped”

42
Q

Stroke Pattern:

“Locked in syndrome”

Loss of horizontal but not vertical eye movements

A

Basilar Artery

Also can be caused by Osmotic Demyelination Syndrome!

43
Q

Stroke Pattern:

Contralateral hemianopia with macular sparing

A

Posterior cerebral artery

44
Q

What is hemiballismus?

Where is the lesion?

A

Sudden, wild flailing of one arm +/- ipsilateral leg.

Contralateral subthalamic stroke (eg. lacunar stroke)

45
Q

What are these?

A

Lewy bodies are abnormal aggregates of protein that develop inside nerve cells in Parkinson’s disease (PD), Lewy body dementia, and some other disorders. They are identified under the microscope when histology is performed on the brain.

46
Q

What are these?

A

Neurofibrillary tangles (NFTs) are aggregates of hyperphosphorylated tau protein that are most commonly known as a primary marker of Alzheimer’s disease. Their presence is also found in numerous other diseases known as tauopathies.

47
Q

What are these?

A

Pick’s disease, is a term that can be used in two different ways. It has traditionally been used as a term for a group of neurodegenerative diseases with symptoms attributable to frontal and temporal lobe dysfunction. Common symptoms that are noticed early on are personality and emotional changes, as well as, deterioration of language.

48
Q

What is the classic triad of “Normal Pressure Hydrocephalus”?

A

Wet, wacky, and wobbly.

Urinary incontinence, cognitive dysfunction, and ataxia.

49
Q

What is Charcot’s triad in the context of MS?

A

Scanning speech

Intention tremor

Nystagmus

50
Q

What are the diagnostic findings in MS?

What are the treatment options for MS?

A

Increased IgG level and myelin basic protein in CSF; oligoclonal bands are diagnostic.

MRI is gold standard; periventricular plaques with preservation of axons.

B-interferon, glatiramer, natalizumab.

Flares treated with IV steroids

Symptomatic treatment for spasms.

51
Q

What type of tumour is this?

Cell of origin? Histological appearance?

A

Meningioma.

Arachnoid cell origin.

Spindle cells concentrically arranged. Psammoma bodies.

52
Q

What neurological pattern of dysfunction is seen in Syringomyelia?

What is Syringomyelia associated with?

A

Syrinx expands and damages the anterior white commisure of spinothalamic tract; bilateral loss of pain and temperature in a cape-like distribution.

Seen in Chiari I malformation

53
Q

What are the neurological findings in Brown-Sequard syndrome?

A
  1. Ipsilateral loss of sensation at the level of lesion
  2. Ipsilateral LMN signs at level of lesion (flaccid paralysis)
  3. Ipsilateral UMN signs below level of lesion
  4. Ipsilateral loss of proprioception, vibration, and light touch below level of lesion
  5. Contralateral loss of pain and temperature and crude touch below level of lesion
54
Q

Pseudopalisading tumour cells on histology and central necrosis and haemorrhage on morphology are suggestive of?

A

Glioblastoma multiforme (grade IV astrocytoma)

55
Q

“Fried egg” cells with a chicken wire pattern and frequent calcifications are associated with?

A

Oligodendroglioma.

56
Q

Concentrically arranged spindle cells with Psammoma bodies are associated with?

A

Meningioma.

57
Q

What is tonotropy as it relates to auditory physiology?

A

Each frequency leads to vibration at a specific location on the basilar membrane;

Low frequency is heard at the apex near the helicotrema

High frequency is heard at the base of the cochlea

58
Q

Damage to the steriociliated cells in the organ of Corti suggests?

Which frequency is lost first?

A

Noise-induced hearing loss.

Loss of high frequency hearing first.

59
Q

Aging-related hearing is referred to as?

Why is low-frequency hearing often preserved?

A

Presbyacusis.

Low-frequency hearing is detected at the apex of the cochlea, in presbyacusis, the base is first to fall victim.

60
Q

Describe the flow of aqueous humour from origin to absorption:

A

Produced by non-pigmented epithelium on ciliary body. Flows into anterior chamber toward trabecular network. 90% of the outflow is through the trabecular meshowork to the canal of Schlemm. 10% goes into the uveoscleral outflow.

61
Q

Describe the pupillary light reflex:

A

Light in either retina is relayed to the pre-tectal nuclei via CN II in the midbrain, that activates BILATERAL Eidinger-Westphal nuclei; pupils then constrict consensually.

62
Q

List the medications which inhibit cytochrome p450:

A

SICKFACES.COM

Sodium Valproate, Isoniazid, Cimetidine, Ketoconazole, Fluconazole, Alcohol, Chloramphenicol, Erythromycin, Sulfonamides, Omeprazole, Metronidazole.

Also grapefruit juice.

63
Q

List the medications which induce cytochrome p450:

A

CRAP GPS (induces me to madness)

Carbemazepines, Rifampicin, chronic Alcohol, Phenytoin

Griseofulvin, Phenobarbitone, Sulphonylureas.

64
Q

What is the mechanism of Baclofen?

What is its clinical use?

A

Activates GABA-B receptors at the spinal chord level, inducing skeletal muscle relaxation.

Muscle spasms and MS.

65
Q

What is the neurotransmitter imbalance seen in Parkinson’s Disease?

What, therefore, are the strategies of pharmacological therapy?

A

Parkinsonism is due to a loss of Dopaminergic neurons and excess cholinergic activity.

  1. Dopamine agonists
  2. Increase Dopamine availability
  3. Increase L-DOPA availability
  4. Prevent Dopamine breakdown
  5. Curb excess cholinergic activity.
66
Q

How does Carbidopa work?

How do Entacapone and Tolcapone work?

A

All 3 increase levels of levels of Dopamine.

Carbidopa is a DOPA decarboxylase inhibitor.

Entacapone and Tolcapone are peripheral and peripheral+central COMT inhibitors.

67
Q

How do Selegiline and Rasagiline work?

A

Both are MAO Type B Inhibitors and so increase central Dopamine.

68
Q

How do Bromocriptine, Pramipexole, and Ropinirole work?

A

All are Dopamine agonists.

Bromocriptine is ergot whereas Pramipexole and Ropinirole are non-ergot.

69
Q

How does Amantidine work?

A

Amantidine reduces Dopamine reuptake and increases Dopamine release.

70
Q

What is the mechanism of action of Opiates?

A

Act as agonists at opioid receptors (mu, kappa, delta) that mediate analgesia at spinal and supraspinal levels. They modulate synaptic transmission by opening K+ channels and closing Ca2+ channels - reducing synaptic transmission.

71
Q

What are the target organs of Alpha-1, Beta-1, and Beta-2 adrenergic drugs?

A

Alpha-1 = Peripheral vasculature, Bladder, Eye

Beta-1 = Heart

Beta-2 = Lungs, Skeletal muscle, Uterus

72
Q

What is first-line therapy for:

Absence seizures?

What is the drug’s mechanism of action?

A

(SUX to have silent seizures)

Ethosuxamide

Blocks thalamic T-type Calcium channels.

73
Q

What is first line and maintenance therapy for:

Status epilepticus?

What are the drugs’ mechanism of action?

A

Benzodiazepines for termination of SE. These increase the acitvity of GABAA by increasing the frequency of Cl- channel opening. (FRENzodiazepines)

Phenytoin for maintenance after termination of SE. These block Na+ channels with zero-order kinetics.

74
Q

What is the first line therapy for:

Partial (clonic) seizures?

What is the drug’s mechanism of action?

A

Carbamazepine

Blocks Na+ channels. Also used for trigeminal neuralgia.

75
Q

What is first line therapy for:

Tonic-Clonic seizures?

What is the drugs mechanism of action?

A

Sodium valproate or Valproic acid.

Increase Na+ channel inactivation and increase GABA concentration by reducing GABA breakdown.

76
Q

How can you prevent vasospasmodic neurolgical sequelae following SAH?

A

Calcium Channel Blockers.

Nimodipine has been shown to reduce M&M following SAH.

77
Q

What are the classical symptoms of organophosphate poisoning?

What is the treatment?

A

DUMBELS (muscurinic activation)

Diarrhoea

Urination

Miosis

Bronchospasm

Emesis

Lacrimation

Salivation

78
Q

What microscopic changes are seen 12-24 hours following ischaemic injury?

A

“Red neurons”

(eosinophilic cytoplasm, pyknotic nuclei, loss of Nissl)

79
Q

What microscopic changes are seen 24-72 hours following ischaemic injury to neurons?

A

Neutrophilic infiltration.

80
Q

What microscopic changes are seen 3-7 days following neuronal ischaemic injury?

A

Macrophage/microglia infilitration and phagocytosis begin.

81
Q

What microscopic and macroscopic changes are seen 1-2 weeks following ischaemic neuronal injury?

A

Reactive gliosis and vascular proliferation around the necrotic area.

Liquefactive necrosis (1 week to 1 month)

82
Q

What microscopic and macroscopic changes are seen >2 weeks after ischaemic neuronal injury?

A

Glial scar formation by astrocytic processes.

Cystic area surrounded by dense glial fibers (>1 month).

83
Q

What is the role of Dynein and Kinesin in the pathophysiology of Herpes Simplex Virus 1?

A

Primary infection involves Dynein-dependent (retrograde) transport of virus to nucleus.

Reactivation involves Kinesin (antegrade) transport of virus down axon to reach skin and mucosa.

84
Q

What is the pathophysiology of Botulism?

A

Botulinum toxin causes disease by inhibiting cholinergic nerves, including both nicotinic and muscarinic receptors.

It enters nerve terminals through endocytosis, where it prevents binding and fusion of Ach containing synaptic vesicles with the plasma membrane.

85
Q

What is the pathophysiology of an acute dystonic reaction?

A

Sudden involuntary contraction of a muscle group is caused by strong Dopaminergic blockade of D2 in the Nigrostriatal pathway. This leads to an excess of cholinergic activity; resulting in extrapyramidal side effects.

M1 receptor antagonists can alleviate symptoms.

86
Q

How does high frequency deep brain stimulation work in Parkinson’s disease?

A

Nigrostriatal degeneration in PD results in excessive excitiation of the GPi by the sub-thalamic nuclei, which in turn causes excessive inhibition of the thalamus.

High-frequency stimulation of the GPi or the sub-thalamic nucleus inhibits firing of these nuclei and alleviates the inhibitory effect on the thalamus.

87
Q

How do the Barbiturates work?

(Phenobarbitol, Pentobarbitol, Thiopental, Secobarbital)

A

Fascilitate GABAA action by increasing the duration (barbiDURATES) of Cl- channel opening, thus decreasing neuron firing.

88
Q

What are Suvorexant and Ramelton?

What are their mechanisms of action?

A

Both are drugs used to treat Insomnia.

Suvorexant is a Orexin/hypocretin antagonist (Orexin is important for wakefullness).

Ramelteon is a melatonin agonist.

89
Q

What is the MAC?

A

The Minimal Alveolar Concentration required to prevent 50% of subjects from moving in repsonse to a noxious stimulus.

90
Q

How does blood:gas partition coefficient relate to induction time?

A

A higher blood gas partition coefficient means a higher uptake of the gas into the blood and therefore a slower induction time.

91
Q

How does Ketamine work?

How does Propofol work?

A

Ketamine blocks NMDA receptors.

Propofol potentiates GABAA

92
Q

How can you reverse non-depolarizing NM blocking drugs?

What are the other considerations when doing this?

A

Neostigmine can be given to compete with the non-depolarizing meds for Ach receptors.

Must be given with Atropine to prevent muscurinic effects such as bradycardia.

USMLE (14 decks)

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