Term
What disorder arises from failure of the rostral neural tube to fuse during development?
What about the caudal neural tube? |
|
Definition
1) Anencephaly (without brain)
2) Spina Bifida (often leading to Arnold Chiari malformation and non-communicating hydrocephalus with increased ICP due to compression on foramen of Magendie and Lushka) |
|
|
Term
| What is the developmental basis for the condition known as "megacolon"? |
|
Definition
| Lack of innervation of colon because of deficient neural crest cell migration (peripheral ganglia and fibers arise from neural crest) |
|
|
Term
| What is the developmental basis for Mesencephaly? |
|
Definition
"Smooth brain," results because of failure of neurons to migrate from ventricles to pia mater.
Often leads to epilepsy |
|
|
Term
| What are the cardinal signs of ICP? |
|
Definition
1) Severe headache (compressed vessels and expansion of dura)
2) Nausea and vomiting (medulla center pressure)
3) Papilloedema (pressure-induced swelling of optic nerve and central retinal artery). |
|
|
Term
| Why do you see a "stiff neck" in patients with Meningitis? |
|
Definition
| Irritation of motor nerves of cervical chord and CN XI. |
|
|
Term
| What is the difference between Communicating and Non-communicating hydrocephalus? |
|
Definition
Both cause high ICP and compression of brain with headache, nausea/vomiting and papilloedema
1) Non-Communicating Hydrocephalus involves an obstruction to flow, such as a tumor or congenital defect (Arnold Chiari Malformation).
2) Communicating hydrocephalus involves either abnormal absorption of CSF by arachnoid granulations into the superior saggital sinus, or overproduction of CSF |
|
|
Term
| What is the first thing you need to worry about if a patient has damage to their blood brain barrier? |
|
Definition
| This means Vasogenic Edema, so you need to keep BP high enough that more fluid is not drawn in. |
|
|
Term
| Which arteries are important for supplying the optic tract? |
|
Definition
1) Anterior choroidal from MCA (also internal capsule)
2) Perforating arteries from ACA (optic tract and chiasm)
** Posterior Cerebral supplies occipital lobe |
|
|
Term
| What functional deficits might you see with a posterior-communicating artery infarction? |
|
Definition
This artery runs the Posterior Cerebral Arteries to the branchesconnects of the internal carotid, forming the circle of willis.
It supplies the mamillary bodies, posterior hypothalamus ad sub-thalamus. |
|
|
Term
| What is the clinical significant of leptomeningeal anastomoses? |
|
Definition
| These Arterial Border Zone Watersheds are particularly susceptible to ischemia and they are the last to be re-perfused |
|
|
Term
| What functional deficits might you see following infarction of the right posterior spinal artery? |
|
Definition
| Supplies right lateral vestibular nuclei (otolith organ information) and Nucleus Solitarious (taste and baroreceptor information) |
|
|
Term
| What are the 6 major clinical presentations and their underlying neurological causes in Wallenberg syndrome? |
|
Definition
Lateral Medullary Syndrome arises because of PICA infarction
1) Hoarse voice and Dysphagia (nucleus ambiguous)
2) Taste deficits (nucleus solitarious)
3) Contralateral pain/temp of body (Spinothalamic)
4) Ipsilateral pain/temp of face (Spinal trigeminal)
5) Ipsilateral Horners (Descending sympathetics)
6) Ipsilateral Ataxia (Inferior cerebellar peduncle) and Vertigo (Vestibular nucleus) |
|
|
Term
| What are the 3 major clinical presentations and their underlying neurological causes in Medial Medullary syndrome? |
|
Definition
MMS arises from anterior spinal infarction.
1) Ipsilateral tongue deflection (Hypoglossal nucleus)
2) Contralateral fine touch (Medial lemniscus)
3) Contralateral hemiparesis (Medullary pyramids) |
|
|
Term
| What are the 5 major clinical presentations and their underlying neurological causes in Paramedian Pontine Syndrome? |
|
Definition
PPS arises because of infarction of paramedian branches of Basilar artery in the Pons.
1) Ipsilateral llateral rectus leading to medial gaze defect (CN VI)
2) Ipsilateral face weakness (CN VII)
3) Contralateral hemiparesis (Corticospinal)
4) Tactile discrimination (Medial lemniscus)
5) Sometimes see ipsilateral Horner's |
|
|
Term
| What arterial infarction could cause expressive aphasia and right hemiparesis? |
|
Definition
|
|
Term
| Infarction of what artery might effect temperature regulation and appetite? |
|
Definition
Hypothalamus
Supplied by posterior communicating artery |
|
|
Term
| What artery supplies the roof of the 4th ventricle? |
|
Definition
| PICA supplies choroid plexus of 4th ventricle as well as all nuclei involves in lateral medullary syndrome. |
|
|
Term
A patient is experiencing valance issues.
What artery supplies cerebellar input from the cortex?
What about cerebellar input from the spinal cord? |
|
Definition
1) AICA (also flocculus (vestibulocerebellum), lateral and inferior cerebellar hemispheres)
2) PICA |
|
|
Term
| What is the difference in blood supply between most brain regions and the Circumventricular organs? |
|
Definition
| The circumventricular organs (Area Postrema, Neurohypophysis and Organum vasculosum) are supplied by fenestrated capillaries, while other areas with BBB are supplied by non-fenestrated capillaries connected to on another by tight junctions. |
|
|
Term
| What are the possible functional consequences of an infarction of the Posterior Cerebral Artery? |
|
Definition
This artery supplies the
1) Thalamus (relay issues)
2) Cerebral peduncle (hemiparesis)
3) Ventral temporal lobe (olfactory issues)
4) Occipital Lobe (contralateral vision issues) |
|
|
Term
| Which artery supplies the fastigial, emboliform, globbose and dentate nuclei? |
|
Definition
These are deep nuclei of the cerebellum, supplied by the superior cerebellar artery.
Fastigial (vermis/motor execution)
Interposed (Intermediate zone/motor execution)
Dentate (lateral cerebellum/motor planning)
**Vestibular nuclei (floculonodular/balance and eye movements) supplied by AICA** |
|
|
Term
| What are the clinical manifestations of Brown-Sequard Syndrome? |
|
Definition
Hemisection of spinal chord leading to
1) Contralateral pain/temp deficit
2) Ipsilateral proprioceptive/tactile/vibration deficits
3) Ipsilateral motor loss |
|
|
Term
| How can you distinguish between different spinal chord levels (i.e. thoracic, cervical, ect.) |
|
Definition
1) White matter decreases from Cervical to Sacral
2) Lateral (autonomic) horns are present at thoracic levels (T1-L3)
3) Ventral horn is largest in Cerical and Lumbar/Sacral levels. |
|
|
Term
| Where do 2nd order cells in the dorsal column/medial lemniscus pathway synapse? |
|
Definition
| These are somatosensory fibers with cell bodies in the gracilus and cuneate nuclei, which ascend to the VPL thalamus (VPM is for face and gets from main sensory and spinothalamic). |
|
|
Term
| How are arms/legs represented in the ascending spinothalamic tract? |
|
Definition
Legs and lateral and Hands/Face are medial.
This distribution mimics that of the medial lemniscus in the open medulla and is opposite to that of the dorsal columns in the spinal chord.
Spinothalamic and Medial lemniscus systems enter the VPL together and then go to S1, where hands/arms are lateral and legs are medial. |
|
|
Term
| What do arterial syndromes affect both the medial lemniscus and corticospinal tracts? |
|
Definition
1) Medial Medullary Syndrome (Anterior Spinal off of Vertebrals)
2) Paramedian Pontine Syndrome (Basilar Branches)
Both from Vertebral-Basilar System |
|
|
Term
| Why is an infarction of the anterior choroidal artery of clinical concern? |
|
Definition
| It supplies the posterior limb of the internal capsule. This is where corticospinal fibers descend and where somatosensory fibers ascend. You can one-sided absense of EVERYTHING that passes through. |
|
|
Term
| Which CN nuclei receive input from VII, XI and X? |
|
Definition
1) Spinal Trigeminal
2) Nucleus Solitarious (taste from VII, IX and X and vascular from IX and X) |
|
|
Term
| Why might you see complete left facial weakness and hyperacusis together? |
|
Definition
Facial Nerve involvement at facial nucleus in Pons.
The nucleus receives bilateral input from the cortex for the upper face and contralateral input for the lower face.
CN VII also innervates stapedius (dampening system in middle ear) |
|
|
Term
| How can you tell between an UMN and LMN lesion causing facial paralysis? |
|
Definition
1) UMN will cause contralateral lower facial weakness because of bilateral input from cortex to upper face regions in facial nucleus.
2) LMN will show ipsilateral complete facial weakness because whole nucleus is knocked out. |
|
|
Term
| Which 2 CN nuclei receive input from both the solitary nucleus and the hypothalamus? |
|
Definition
1) Superior salivatory (CN VII, lacrimal, submandibular and sublingual).
2) Inferior Salivatory (CN IX, parotid) |
|
|
Term
| Why might you see difficulty with vocalization and swallowing in a patient? |
|
Definition
Nucleus ambiguous lesion (gets IX and X and input from Solitary nucleus)
** Located between Spinal Trigeminal nucleus and inferior olivary complex** |
|
|
Term
| What is the course of CN fibers that convey pain/touch/temperature information from the posterior 1/3 of the tongue? |
|
Definition
| These of GSA and GVA fibers of CN IX that joint the spinal trigeminal and main sensory nuclei of CN V, before giving rise to axons that cross the midline to trael with the contralateral medial lemniscus and spinothalamic tracts into the thalamus. |
|
|
Term
| What is the functional role of the Dorsal Motor Nucleus of CN X? |
|
Definition
Receives chemoreceptor/baroreceptor input from CN IX (carotid body) and CN X (aortic body) via Solitary Nucleus and innervates
1) Heart (decrease rate with Ach)
2) Esophagus (increase peristalsis)
3) Epigastrium (gastric secretion)
4) Lungs (constriction) |
|
|
Term
| What is the anatomical basis for the development of Horner's syndrome during PICA infarction? |
|
Definition
1) Descending sympathetics from hypothalamus usually enter intermediolateral cell column of spinal chord and then exit to synapse in cervical chain ganglia
2) Post-ganglionic sympathetics innervate Levator palpebrae (Ptosis), Ciliary ganglion smooth muscle (myosis) and sweat glands (Anhydrosis) |
|
|
Term
| What 4 "M" structures that are located along the midline of the brainstem and their associated deficits? |
|
Definition
1) Motor tract (contralateral weakness of arm/leg)
2) MLF (Ipsilateral Interocular Opthalmoplegia)
3) Medial Lemniscus (Contralateral vibration/touch)
4) Motor Nuclei (3,4,6,12) (Ipsilateral) |
|
|
Term
| What 4 "S" structures that are located along the lateral surface of the brainstem and their associated deficits? |
|
Definition
1) Spinothalamic tract (Contralateral pain/temp)
2) Sympathetic tract (Ipsilateral Horner's)
3) Spinocerebellar (Ipsilateral ataxia of arm/leg)
4) Sensory N. of V (Ipsilateral pain/temp of face) |
|
|
Term
| What is the clinical presentation of a lacunar infarct of the left MLF? |
|
Definition
| Left internuclear ophthalmoplegia with failure of adduction of left eye and right eye nystagmus during head turn to right |
|
|
Term
| What are the 3 muscles innervated in the eyelid and their clinical significance? |
|
Definition
1) Drooping eyelid (Levator Palpebri from CN III)
2) Eyelid can't close (Orbiculus oculi from CN VII)
3) Ptosis in Horners (Superior tarsal from Sympathetics) |
|
|
Term
61 year old patient with resting tremor of left hand cannot swing left arm when he walks and has reduced facial animation.
He seldomly blinks and has rigidity in the left arm as well.
What is going on? |
|
Definition
|
|
Term
46 year old presnts with difficulty ascending stairs and must pull herself with the handrail.
She can't lift objects into kitchen cupboards and keeps her arms up in the air to fix her hair.
What is going on? |
|
Definition
Proximal muscle weakness in arms and legs suggests Myopathy.
No reflex issues, so AHN and Nerve are out as far as LMN issues go. IF this was NMJ issue, you might not see this proximal distribution. |
|
|
Term
| How can you tell between Anterior Horn and projecting Nerve involvement in lower motor neuron syndromes? |
|
Definition
Symmetry!
Both will have decreased reflexes, bulk and no myotonia.
Both should present with fasciculations, but ANH will be asymetric while Nerve will be symetric. |
|
|
Term
| How can you tell between NMJ and Myopathy issues in LMN syndromes? |
|
Definition
Myopathy will often present with myotonia and a proximal distribution.
NMJ will not have myotonia |
|
|
Term
| What time of LMN disorder presents with sensory involvement? |
|
Definition
| Nerve disruption is only case. |
|
|
Term
| How can you tell between UMN and LMN syndromes? |
|
Definition
UMN has increased reflexes (positive Babinski), increased tone, minimal Atrophy, Clonus and hemiparesis.
LMN has decrease in muscle bulk (atrophy), dampened DTRs, Fasciulations, weakness and decreased tone. |
|
|
Term
22 year old presents with disorientation and agitation, but without motor weakness or language-loss
What is most likely going on? |
|
Definition
| Sounds like Encephalopathy (no sub-cortical involvement). |
|
|
Term
A patient experiences what feels like an "electric shock" every time that they flex their cervical spine.
What is going on? |
|
Definition
Lhermitte's phenomenon
DOrsal column dysfunction in cervical region |
|
|
Term
75-year old man developed weakness of right arm and leg and slurring of speech. He has difficulty seeing with right eye.
Exam reveals hemiparesis and right lower facial muscle weakness, but eye closure and forehead elevation were normal (right peripheral visual field defect present).
What is going on? |
|
Definition
| Left hemisphere motor tract lesion (Broca's and contralateral hemiparesis with lower facial weakness). |
|
|
Term
69 year old diabetic, hypertensive female notes imbalance with left-veering gate. She complains of right-side numbness and exam reveals incoordination on left and reduced pinprick sensation on left face and right body.
Whats going on? |
|
Definition
Left Medullary Syndrome (PICA)
1) Crossed dorsal column signs suggest left brainstem issue
2) Left gait suggests left spinocerebellar issue |
|
|
Term
| How do patients with Cerebellar issues typically present? |
|
Definition
1) Gait ataxia
2) Extremity and speech incoordination
3) Nystagmus |
|
|
Term
| What is the difference between Dysarthria and Dysphonia? |
|
Definition
1) Dysarthria is slurring of speech, usually occurring with Cerebellar involvement
2) Dysphonia is crackling/hoarseness, usually occurring with Vagal innervation issues. |
|
|
Term
| When mighty you see pain specifically when a patient begins to walk? |
|
Definition
| Spinal root involvement (Neurogenic claudication) |
|
|
Term
| Why is PET-CT so good for the head and neck? |
|
Definition
| Spatial resolution of CT with physiological information from PET. |
|
|
Term
When should you use each of the following modalities?
1) CT
2) MR
3) Myelography
4) PET |
|
Definition
1) Screening tool (cheap) with good resolution for bone
2) Subtle differences in soft tissue. Safe. Multiple phase sequences (T2 for CSF). Not restricted to axial plane).
3) Inject contrast into thecal sac to look at bone for surgical planning.
4) Source of seizures, tumor vs. scar. |
|
|
Term
| What different phase pulses are available for MRI and why are they used differentially? |
|
Definition
T1- clarify anatomy (black CSF)
T2- CSF is bright
FLAIR- T2-variant for pathology gets rid of water signal
DWI for stroke |
|
|
Term
| What are the contraindications for contrast use? |
|
Definition
1) Heart failure because dye is hyperosmolic (fluid bolus)
2) Allergies
3) Renal toxicity for iodinized dyes. |
|
|
Term
| How can the ventricle:sulci ratio be used clinically? |
|
Definition
If it is high, you are looking at pathology (hydrocephalus).
Larger sulci and ventricles are normal in adults, but increased ratio is not. |
|
|
Term
| Which artery comes off of the Carotid siphon? |
|
Definition
|
|
Term
What pathology presents as Lentiform clot?
What about Crescentic?
Along falx cerebri?
What should be done in each case? |
|
Definition
1) Lentiform is epidural hematoma from middle meningeal artery. RUSH TO ER
2) Crescentic is subdural from venous rupture- watch closely
3) Also Sudural (falx cerebelli and tentorium cerebelli also possible) |
|
|
Term
| What do "straight lines" separating norma and abnormal brain tissue on CT/MRI suggest? How does this arise? |
|
Definition
Edema in region supplied by singular artery.
Without glucose, Na/K pumps cannot function and Na+ runs into cells, causing them to swell and lyse. |
|
|
Term
| A patient presents with a blown left pupil. Why do you RUSH him to the OR? |
|
Definition
| Could be Uncal Herniation through tentorium cerebelli. Death follows! |
|
|
Term
| How does Myelin increase speed of conduction? |
|
Definition
| By reducing membrane capacitance, and thus minimizing the amount of local current required to depolarize neurons to threshold. |
|
|
Term
| What types of cells give rise to Glioblastoma multiforme tumors? |
|
Definition
| Germinal Zone Astrocytes (neural stem cells) that arise from Radial Glial Cells |
|
|
Term
| What cell types arise from Radial Glial Cells? |
|
Definition
RGCs come from neuronal epithelium of neural tube and differentiate into
1) Oligodendrocytes
2) Astrocytes (parenchymal)
3) Ependymal cells (BBB)
4) Germinal-zone astrocytes |
|
|
Term
| What are the 6 primary functions of Astrocytes? |
|
Definition
BEST BF
1) BBB (end-feet envelope capillary endothelium (function and repair)
2) Energy/Metabolism (take up glucose from neurons and produce metabolites to pass through tight junctions, as well as store Glycogen for hypoglycemic states)
3) Synapse formation/maintenance (thrombospondin and guidance cues)
4) Tissue Repair (gliosis with hypertrophy, proliferation and scar formation)
5) Blood flow (NO, prostaglandins, AA for neurovascular coupling)
6) Fluid balance/edema (Aquaporin 4 for water balance, NO and VEGF for permeability) |
|
|
Term
| Where are microglia derived from and what is their primary function? |
|
Definition
1) Yolk sac and Bone marrow monocytes
2) Early microglia have ameboid movement become resting, ramified microglia (immunosurveilance)
- Once activated, these microglia retract/thicken their processes and develop ability to phagocytose |
|
|
Term
| How can microglia contribute to CNS pathology? |
|
Definition
1) Gliosis from chronic activation leads to inflammatory tissue damage.
2) In HIV, activated microglia cause dementia
3) In AD, beta-amylodi peptides activate microglia and cause injury to degenerating neurons. |
|
|
Term
| What are the different roles of Astrocytes in synaptic function? |
|
Definition
1) Growth guidance
2) Pruning (C1q tagging for microglia)
3) K+ sequestration
4) NT clearance (glutamate and GABA)
5) Gliotransmission (tripartite synapse) |
|
|
Term
| How do synapses at the NMJ differ from those in the CNS? |
|
Definition
| They always generate APs! |
|
|
Term
| When are Ascorbic acid and B6 critical for neuronal transmission? |
|
Definition
1) Ascorbic acid is for Dopamine-beta-hydroxylase to make NE from Dopamine INSIDE synaptic vesicle
2) B6 is co-factor for dopa decarboxylase to make Dopamine from L-Dopa |
|
|
Term
| How do you calculate E-EPSP? |
|
Definition
|
|
Term
| What are the Sympathetic and Parasympathetic neuron distributions? How does Ach signaling relate to this? |
|
Definition
Ach is pre-ganglionic input to BOTH (global drugs will therefore hit both)
Symp= T1-L3
Para= CN 3,5,9,10 and S1-S4 |
|
|
Term
| How is Ach synthesis and vesicle-packing achieved? |
|
Definition
1) Choline uptake via Na-dependent transporter (RLS) and jointed with acetyl-coA via ChAT to form Ach and coA.
2)ATP-dependent process utilizing H+ pump gradient. |
|
|
Term
| Explain the differential use of the 2 types of NMJ blockers. |
|
Definition
1) Depolarizing (Succinylcholine- RAPIDLY REVERSIBLE) blockers bind to and open channel, initially causing fasiculations (not degraded by AchE), but are then followed by flaccid paralysis
2) Competitive blockers such as Curare (d-tubocurarine, pancuronium) compete for Ach binding site (only need to bind 1 site!) |
|
|
Term
| To what nACh receptors does Nicotine bind? |
|
Definition
Those containing B2 (Brain and Peripheral ganglia).
Cause calcium boost?? |
|
|
Term
| Why might you use a mAChR antagonist clinically? |
|
Definition
| Atropine/Scopolamine for anesthetic pre-medications, COPD, PD, mushroom toxicity, ect. |
|
|
Term
| How might you treat Myasthenia gravis? |
|
Definition
Autoimmune disease that attacks nAchRs at NMJ.
Treat with AChE inhibitor |
|
|
Term
| What is the medication "Chantix"? |
|
Definition
| Partial agonist of nAChR used to treat smoking (also causes depression) |
|
|
Term
| How do Benzodiazepines exert their effects? |
|
Definition
Increase GABA affinity for GABAa-R.
- Subunit specific action (alpha2-anxiolitic, alpha1 is amnestic)
- Inhibit with flumazenil
Examples include diazepam (Valium), Versed and Xanax |
|
|
Term
| How do Barbiturates exert their effects? |
|
Definition
Reversibly depress neuronal activity via GABAa-R by binding to distinct sites and DIRECTLy activating the receptor.
DANGEROUS when used with other CNS depressants such as alcohol
Examples include Brevital, Nembutal, Luminal and Petothal |
|
|
Term
| How do General anesthetics exert their effects? |
|
Definition
Potentiate GABA effects on GABAa-R (like benzos) with subunit-specificity
Examples include Propofol and Etomidate |
|
|
Term
| What are the current drugs of choice for treating insomnia? |
|
Definition
Benzodiazepine-like compounds (Ambien, Sonata, Lunesta) that also potentiate GABA binding to GABAa-R
Sleep driving! |
|
|
Term
| How do Local Anesthetics work? |
|
Definition
Analine/Benzoic acid based molecules linked to tertiary amine via Ester (procaine) or amide (lidocaine).
Bind voltage-gated sodium channels in dose-dependent (un-competitive) manner and stabilize closed confirmation.
Block pain fibers first, then cold, then hot, then deep pressure then motor (mantle>> core) |
|
|
Term
| What are some down-sides to using local anesthetics? |
|
Definition
1) Non-specific action on all tissues with VG-sodium channels (heart and CNS neurons)
- many cells are inhibited by synaptic input, so you could "remove break"
- with Epi can cause cardiac arrest
- Hypersensitive to esters or Epi |
|
|
Term
| Explain the relationship between pKA and local anesthetic action. |
|
Definition
1) LA pKA is where 50% are lipid soluble and 50% are water soluble
2) LA pKA> physiological pH, so more exists in water-soluble form when injected.
If you lower PH, even more will be acidic, and more toxic! |
|
|
Term
A patient presents with elevated thresholds for two-point discrimination on the left lower half of the body.
What artery may have been damaged? |
|
Definition
This is fine touch (A-beta fibers of left dorsal column), which is supplied by the left posterior spinal artery.
As it ascends into the brainstem and becomes the medial lemniscus, it is supplied by anterior spinal artery as well |
|
|
Term
A patient presents with absent pain/temperature sensation on both arms.
What could be going on? |
|
Definition
The bilateral spinothalamic involvement suggests involvement of anterior commissure, where fibers are crossing.
Syringomyelia would explain this, with the degenerating central canal impinging upon the white commissure. |
|
|
Term
A patient presents with left-side sensory neglect.
What is going on? |
|
Definition
| Lesion to right posterior parietal cortex |
|
|
Term
| What is the difference between the types of pain carried by A-delta and C fibers? |
|
Definition
1) A-delta is well-localized, 'fast' pain that responds to high-intensity stimulation
2) C is slower, more persistent and unpleasant pain with thermal and chemical response (Polymodal)
- They have low "safety factor," because little damage is needed to prevent sodium conduction** |
|
|
Term
| How does pain transduction occur in nociceptors? |
|
Definition
Chemical Intermediary, Sensitization and Antidromic Axon travel
1) Tissue damage leads to release of K+, 5-HT, Bradykinin and Prostaglandins, which act on nerve terminals.
2) Nerve terminals release Substance-P (same fibers that are inhibited by descending RF fibers) and stimulate mast cells to release Histamine.
3) Axon reflex with antidromical signal travel backwards and spreads to other peripheral branches causing a vasomotor response |
|
|
Term
| What is the structure of the ventral horn and its main projections? |
|
Definition
1) Posteromarginal Zone (PMZ) gets nociceptive A-delta and C-fibers, and projects across midline to ascending spinothalamic tract and ascends mono-synaptically to the thalamus.
2) Substantia Gelatinosum (deep to PMZ) contains local interneurons, which receive input via reticulospinal pathways and nociceptive pathways (NATURE of pain)
3) Nucleus Proprius receives input from A-beta, A-delta and C-fibers, as well as inhibitory fibers from SG (Wide Dynamic Range Cells). It crosses midline and ascends poly-synaptically as Spinoreticulodiencephalic tract. |
|
|
Term
What is "Wind up" and how does it develop post-operatively?
How do you avoid it? |
|
Definition
1) C-fibers release glutamate that binds NMDARs and leads to central sensitization of pain circuits in spinal chord
2) Give LA (lidocaine or Novocain) during surgery. |
|
|
Term
| How does "neurogenic pain" in Thalamic Pain Syndrome develop? |
|
Definition
Lesions to posterior thalamus (maybe from Posterior Cerebral Artery infarction) leads to pain without peripheral source.
The posterior thalamus receives spinothalamic, medial lemniscus and spinal trigeminal input. |
|
|
Term
| How is control of pain achieved by descending neurological pathways? |
|
Definition
1) The NP projects to the brainstem RF via the spinoreticulodiencephalic pathway.
2) The RF gives off serotonergic reticulospinal neurons that stimulate ENK-releaseing cells (inhibited by Naloxone)
3) ENK inhibits NP cells and Substance-P releasing C fibers (sparing low-threshold A-beta fibers) |
|
|
Term
| What defines a "sensory unit"? |
|
Definition
A dorsal root ganglion cell, including all of its peripheral and central branches and its associated receptive ending
No dendrites |
|
|
Term
Explain how afferent inhibition enhancement of two-point discrimination occurs in the cuneate nucleus.
What is the relevance of the "temporal component" of this afferent inhibition? |
|
Definition
1) Local inhibitory neurons are activated by stimulated cells within a given receptive field, leading to powerful PRE-synaptic inhibition of adjacent cells.
2) Slow-decaying IPSP compared to EPSP gives a Temporal Component which "cleans up" the signal in space and time. |
|
|
Term
| Why might "shaking your thumb" after burning it reduce pain? |
|
Definition
Increase activation of A-beta fibers in comparison to A-delta and C-fibers in Substantia Gelatinosa in Posterior Horn of SC.
A-beta activation in SG leads to Inhibition of NP. |
|
|
Term
| What are the 2 major pain-processing pathways in the spinal cord? |
|
Definition
1) Spinothalamic (gets inputs mostly from contralateral PMZ of dorsal horn) projects mono-synaptically to thalamus
FAST, PRICKING PAIN
2) Spino-reticulo-diencephalic (gets inputs mostly from NP of dorsal horn) projects poly-synaptically to brainstem RF, thalamus and hypothalamus (limbic projection). SLOW, BURNING PAIN |
|
|
Term
| How can you tell between conductive and sensorineural hearing loss? |
|
Definition
Weber and Rinne Tests
1) Weber on top of head (if lateralizes to unaffected ear, it is conductive)
2) Rinne on mastoid then on ear (conductive is Bone > Air) |
|
|
Term
| Where is endolymph made and how does it contribute to sound transduction? |
|
Definition
1) High K/low Na fluid made in Stria Vascularis of Scala Media (125mV potential difference between endolymph and perilymph maintained by Na/K/2Cl- channels)
2) Sound-evoked vibration of tympanum causes deflection of Basilar membrane, causing movement of hair cells in Organ of Corti (stereocilia are embedded within tectorial membrane and exposed to endolymph, while cell bases are bathed in perilymph)
3) Deflection of stereocilia towards longest cilia opens mechano-gated ion channels via tip-links, and potassium flows in because of negative potential generated in 1
4) Depolarization, calcium influx, ca-gated K channel opening and glutamate release onto bipolar neurons of CN VIII |
|
|
Term
| Why is use of Aminoglycosides, Aspirin and Loop Diuretics such as Furosemide (Lasix) dangerous? |
|
Definition
Hearing damage
1) Aminoglycosides enter mechano-gated ion channels and kill hair cell
2) Aspirin can cause Subjective Tinnitus
3) Lasix blocks Na/K/2Cl transported expressed by Stria Vascularis that are responsible for maintaining Endocochlear potential for signal transduction. Can be permanent if cells die. |
|
|
Term
| What are Otoacoustic Emissions and how are they used clinically? |
|
Definition
Measure of Cochlear function through outer hair cell (OHC) activity.
OHCs sharpen frequency tuning by amplifying low-intensity movements of the Basal membrane in response to sound. |
|
|
Term
| How is noise reduction in the cochlea achieved following cell-induced damage? |
|
Definition
Olivocochlear pathway
Gain reduction of outer hair cells through SOC efferents that release Ach to hyperpolarize them (leading to their lengthening).
Remember, 95% of afferents arise from base of inner hair cells (thick, myelinated) and 5% from outer hair cells (thin, unmyelinated) |
|
|
Term
| What types of information are encoded by Type 1 fibers of CN VIII arising from Spiral Ganglion? |
|
Definition
These fibers trave in body modiolus to Cochlear nucleus
1) Spatial Code- organized tonotopically within CN VIII by Characteristic Frequency
2) Temporal Code- Phase-locked
3) Loudness- Amplitude of sounds determines amount of NT release by Hair Cells onto Spiral ganglion cells of CN VIII, which determines firing rate onto Cochlear Nucleus (i.e. loudness) |
|
|
Term
| How is sound localization achieved by the auditory system, despite having only information about frequency, time and amplitude? |
|
Definition
LSO (IID- important for High-frequency sound) and MSO (ITD-important for Low-frequency sound)
After CNVIII fibers synapse on cochlear nucleus (CN) and ascend in dorsal, intermediate and ventral stria, they synapse in SOC (then then proceed to central nucleus of IC via lateral lemniscus, the MGN of the thalamus and A1).
1) MSO receives excitatory input bilaterally from cochlear nuclei and compares timing to determine inter-aural time difference
2) LSO receives excitatory input from ipsilateral CN and inhibitory input from contralateral CN via the MNTB (through calyx of held synapse in MNTB) |
|
|
Term
| What types of Auditory Evoked Potentials (AEPs) exist and how are they used clinically? |
|
Definition
Used to detect hearing loss in Kids and Infants
1) ABR at 1.5-15ms
- waves 1 and 2 are CN VIII
- wave V is lateral lemniscus and IC
2) Middle Latency Response (MLF) at 25-50ms
- NA (negative) waves following ABR from upper brainstem/auditory cortex
- PA waves from A1 bilaterally |
|
|
Term
| What is the functional importance of the Eustachian tube? |
|
Definition
| Exchanges pressure (i.e. when plane goes up) and can cause disease if clogged |
|
|
Term
| What is the clinical importance of a mutation in Cadherin-23? |
|
Definition
| Congenital Deafness because of absent tip-link protein for stereocilia |
|
|
Term
| How can you immediately tell between Central and conductive/sensorineural hearing loss? |
|
Definition
| Central NEVER presents monaurally, since innervation has converged at this point in the pathway. |
|
|
Term
| What do Endocanabinoids have to do with Tinnitus? |
|
Definition
| Endocanabinoid receptors are down-regulated in the VCN, leading to less inhibition and greater excitation. |
|
|
Term
What visual deficits would each of the following cause in a patient?
1) Lesion to left optic nerve
2) Lesion to optic chiasm
3) Lesion to right optic tract
4) Lesion to Left Meyer's Loop
5) Lesion to Posterior limb of internal capsule
6) Tumor in the temporal lobe
6) Lesion to Cuneate gyrus |
|
Definition
1) Left eye blindness (could only get info from left visual field)
2) Bitemporal Heteronymous Hemianopsia (lose both nasal fields as they cross)
3) Contralateral Homonymous Hemianopsia (right temporal and left nasal hemiretina representing the left visual hemifield.
4) Contralateral Homonymous Superior Quandrantanopsia (where fibers of lingual gyrus travel representing right superior quandrant)
5) Inferior Quandrantanopsia (all fibers heading to Cuneate gyrus travel through here)
6) Superior Quandrantanopsia (this is where Meyer's loop travels before turning caudally towards the lingual gyrus)
7) Inferior Quandrantanopsia |
|
|
Term
| Why do you see papilloedema in cases of high ICP? |
|
Definition
| Compression of central retinal artery arising from opthalmic artery off the the internal carotid. |
|
|
Term
| How does Phototransduction occur at the retina? |
|
Definition
1) Rhodopsin pigment breaks into retinal and opsin
2) Retinal activates PDE, which cleaves cGMP and increases Na+ permeability
3) If depolarization is great enough (greater change in light intensity, greater change in Vm) to generate an action potential and release NT to ganglion cell exiting retina |
|
|
Term
| How is Stereopsis (depth perception) achieved in the visual pathway? |
|
Definition
The first "Binocular" neurons are found in area 17, where projecting ocular dominance columns of different eyes from layer IV synapse on the same neurons in layer II/III or layer IV.
These cells now have information from BOTH eyes. |
|
|
Term
How is contour orientation coding achieved in the visual cortex?
How does this organization relate to mapping in area 1,2,3? |
|
Definition
1) Converging sets of LGN afferents with adjacent receptive fields on the retina form "elongated" receptive fields in area 17.
This orientation confers sensitivity to bars or edges oriented parallel to long axis of receptive fields.
Cells with the same orientation preferences are found together in the same cortical columns (adjacent columns map slightly different orientations)
2) In somatosensory cortex you find a similar columnar organization, with cells in the same column responding to the same modality and sharing receptive fields (4 modality-specific body maps in somatosensory cortex) |
|
|
Term
How might a patient end up with the following visual defects?
1) Lack of color vision
2) Visual Agnosia of behaviorally relevant stimuli
3) Sensory Neglect |
|
Definition
These are Extra-striate deficits, which are Perceptual NOT Visual (sort of the equivalent of an Apraxia)
1) V4 at occipitotemporal junction
2) Inferior Temporal Cortex
3) Contralateral posterior parietal cortex. |
|
|
Term
What is the definition of a stroke and how does it typically present?
What else should be on your differential? |
|
Definition
1) Sudden neurological deficit caused by a vascular problem
2) Tingling, numbness, weakness slurring of speech, double vision
3) TIA (<24h), Migraine, Seizure, Facticious |
|
|
Term
A patient presents with Unilateral weakness, numbness and tingling, as well as monocular vision loss in the right eye and gaze deviation to the left. He says they came on suddenly.
They are having difficulty speaking and when they are asked to draw a clock, they only draw the left side.
What is going on? |
|
Definition
A left anterior circulation infarction fits, perhaps to MCA.
Broca's aphasia gives you left lateralization, and monocular loss of vision and non-dominant sensory neglect are suggestive of anterior circulation.
Gaze to affected side is consistent, because left frontal eye field is not projecting affectively to right PPRF, which is therefore unable to cause contraction of right LR and left MR to turn eyes to right.
Sounds like a stroke that is affecting Broca's area (left inferior frontal gyrus) and vision of the right eye (left frontal eye field?). There is right side-neglect, indicating a left parietal lobe issue and a gaze deviation to the left. |
|
|
Term
| Why would a patient with with a stroke affecting the left posterior circulation have a gaze deviation to the right? |
|
Definition
Ant vs. Post is a matter of FEF vs. Pons involvement
If the lesion affected the left Pons, for example, you might lose the left PPRF, which projects to the left IV nucleus.
This nucleus leads to contraction of the left lateral rectus and right medial rectus muscles, turning the eyes to the left. If it is gone, the eyes will gaze towards to the RIGHT, away from the side of the lesion. |
|
|
Term
A patient presents with the sudden "worst headache of their life"?
What should you do? |
|
Definition
This is probably a sub-arachnoid hemorrhage, until proven otherwise, which is a dangerous arterial bleed that requires immediate attention.
It is most likely a busted Aneurism in the circle of willis, and must be repaired to prevent re-bleeding. |
|
|
Term
| When considering stroke in your differential, what may CT miss and how can you correct for this with further testing? |
|
Definition
CT will miss small, sub-arachnoid hemorrhages and early Ischemic strokes.
1) For the SAH, do an LP below L1-L2
3) For ischemic stroke, get an MRI (DWI) |
|
|
Term
| What are the 3 major types of strokes, their most important risk facts, and their course of prevention/treatment? |
|
Definition
1) Ischemic
- Hypertension, Atherosclerosis, Cardioembolism, Small Vessel Disease (blood flows slowly, clots form and embolize)
- Give TPA within 3 hours
2) Intracerebral
- Hypertension, Arteriovenous malformation, Amyloid Angiopathy
- STOP bleeding
3) Sub-arachnoid hemorrhage
- Berry Aneurism, Trauma
- Repair Aneurism to prevent re-bleeding. |
|
|
Term
| Why is a Subdural hematoma generally less worrisome than an Epidural hematoma or Sub-arachnoid hemorrhage? |
|
Definition
| Sub-d hematoma is a rupture of bridging veins around superior saggital sinus, a system that is under MUCH less pressure than the arterial systems that are ruptured in the other 2 cases. |
|
|
Term
A patient presents with a blown left pupil.
Why are you worried and what are the possible explanations? |
|
Definition
Remember, CN III is important for pupillary constriction, acting through parasympathetic fibers that pass through the ciliary ganglion and enter the iris sphincter muscle
1) UNCAL herniation through tentorium cerebellum would compress CN III, the posterior cerebral artery (contralateral visual defect) and the contralateral cerebral peduncle (ipsilateral weakness).
2) Other causes of CNIII compression could also explain the symptoms. |
|
|
Term
| What is the most common cause of non-traumatic intra-parenchymal hemorrhage and where do these strokes most often occur? |
|
Definition
1) Hypertension
2) Deep gray matter structures such as Basal Ganglia, Pons and Cerebellum (mini-aneurisms in lipohyalurinic vessels) |
|
|
Term
| Where to AVMs most commonly cause intraparenchymal strokes and in what population? |
|
Definition
MCA of young (2nd-4th decades) patients.
Can also cause SAH |
|
|
Term
| What is a cause of Non-hypertensive intraparencymal stroke that occurs most commonly in elderly people? |
|
Definition
| Amyloid angiopathy causes weakened vessels that lead to "lobar hemorrhages" to cerebral cortex and subcortical white matter |
|
|
Term
| Which types of cells are most susceptible to Global Ischemia in adults? |
|
Definition
GluR mediated hypoxic damage (excitotoxicity)
1) CA1 neurons in hippocampus
2) Purkinje fibers in Cerebellum
3) Layer III, IV neurons |
|
|
Term
| Describe the progression of a focal ischemic infarct resulting from Watershed infarcts, Embolic Disease or Small Vessel Disease. |
|
Definition
1) Acute (48h) brain gets soft, edematous with blurring gray-white junction
2) Subacute (2-14d) brain gets liquifactive necrosis
3) Chronic (weeks to months) cystic cavity forms |
|
|
Term
| What are the 5 sub-areas of motor cortex and how do lesions to these areas manifest clinically? |
|
Definition
1) Supplementary Motor (area 6)- Planning of complex motor sequences
- Can't execute complex movements
2) Pre Motor (area 6)- Planning and execution of sensory-guided behavior (input from basal ganglia)
- finger to nose
3) Primary Motor Cortex
- Contralateral paresis/paralysis
4) Frontal Eye Fields
- Contralateral gaze defect (goes through PPRF to contralateral IV nucleus)
5) Broca's Area
- Expressive aphasia |
|
|
Term
| What are the 3 sub-areas of Basal Ganglia and how do lesions to these areas manifest clinically? |
|
Definition
1) Caudate/Putamen/Globus Pallidus (Huntington's chorea)
2) Substantia Nigra (Parkinson's)
3) Sub-thalamic nucleus (Hemiballismus) |
|
|
Term
| What are the primary differences between the laterally and medially running motor tracts in the spinal chord? |
|
Definition
1) Lateral is most distal musculature and exit at 1 or a few segmental levels (Lateral Corticospinal and Rubrospinal)
2) Medial is for axial/proximal musculature for postural adjustment and exist at multiple segmental levels (Vestibulospinal, Tectospinal, Reticulospinal, Anterior Corticospinal) |
|
|
Term
| What is the structure/innervation of a muscle spindle? What is its primary function? |
|
Definition
Sense changes in length.
1) Groups of intrafusal fibers in fluid-filled capsule
2) Sensory innervation by 1a (change in length) and II (absolute length) afferents, which exit and enter the spinal chord through a dorsal root ganglia.
3) Motor innervation by y-motonuerons (Fusimotor) that effect primary and secondary spindle afferents. |
|
|
Term
| What is the difference between a Motor Unit and a Motor Pool? |
|
Definition
1) Motor Unit is single motoneuron with the group of muscle fibers it innervates
2) Motor Pool is group of motonuerons recruited for a single whole muscle. |
|
|
Term
| What is the structure/innervation of a Golgi Tendon Organ? What is its primary function? |
|
Definition
Sensitive to muscle stretch (tension)
1) Located at the ends of extrafusal fibers, between muscle and bone/tendon of insertion, and "in series"
2) Sensory innervation by Group 1b fibers
3) Motor innervation of Extrafusal fibers is alpha motoneurons. |
|
|
Term
| Explain how the Patellar DTR works. |
|
Definition
Resist changes in muscle length imposed by environment, increasing Tone.
1) Tap with hammer causes passive muscle stretch, which excites 1a spindle afferents that synapse on motoneurons in the ventral horn of the spinal chord (going in through dorsal roots).
2) 1a fibers mono-synaptically excite homonymous motoneurons and synergistic motoneurons and di-synaptically inhibit antagonist muscles.
** remember, during walking, alpha and gamma motoneurons are excited together to maintain sensitivity to small changes in muscle length** |
|
|
Term
| Explain how the inverse myotatic reflex works. |
|
Definition
Dampens contraction in response to stretch, allowing further stretch.
1) Excites group 1b GTO afferents that synapse on ventral root motoneurons.
2) Poly-synaptically excite antagonist muscles and poly-synaptically inhibit homonymous and synergistic muscles. |
|
|
Term
| What is the role of the myotatic and inverse myotatic reflexes in voluntary movement? |
|
Definition
Modulated by Reticulospinal System (facilatory and inhibitory RF in pons and medulla that are controlled by the cortex).
1) Stretch reflex counteracts changes in joint positon by making muscles stiffer
2) GTO reflex maintains muscle tension as muscle fatigues. |
|
|
Term
| What are the primary differences between the Lateral and Anterior Corticospinal Tracts? |
|
Definition
1) LCS crosses at medullary pyramids and controls distal musculature (exiting at one or a few spinal segments)
2) ACS crosses at multiple segments of innervation in spinal chord and innervates proximal/axial muscles for postural support. |
|
|
Term
| How might a lesion of fibers traveling from the cortex to the inhibitory reticular formation in the medulla influence Spinal chord reflexes? |
|
Definition
This is an example of Diaschisis and would result in heightened reflexes in anti-gravity muscles leading to Decorticate posture (Extended leg at hip and knee, and Flexed arm)
1) The cortex inhibits cells the facilitatory RF and excites cells in the inhibitory medullary RF area.
2) Without these projections, there would be less inhibition of the spinal chord via the Reticulospinal tract, and uncontrolled excitatory input from the Vestibular system. |
|
|
Term
| What major features differ between an UMN and LMN lesion? |
|
Definition
1) UMN presents with paralysis and spasticity (Spastic Paralysis- anti-gravity, unidirectional and velocity-sensitive) and a present Babinski reflex
2) LMN presents with paralysis and hypotonia (Flaccid Paralysis) and hyporeflexia. |
|
|
Term
| How would a lesion restricted to M1 present? |
|
Definition
Flaccid Paralysis with + Babinski (otherwise, if more extensive, presents as spastic, because UMN issue)
**may reflect direct contact with motoneurons made by area 4** |
|
|
Term
| Why do central lesions initially cause Flaccid paralysis, but later develop into Spastic paralysis? |
|
Definition
Similar pattern is seen with pre-ganglionic sympathetic and parasympathetic neuron damage with BP.
1) Increased sensitivity of spinal cord interneurons or motoneurons to remaining synaptic inputs
2) Sprouting of collaterals from 1a reflex arch afferent system |
|
|
Term
| What the difference between Area 4 and Areas 1,2,3 in terms of information coding? |
|
Definition
Remember, Area 4 is thickest level of cortex, with sparse layer IV cells and huge (Betz) layer V cells.
1) Area 4 is NOT modality specific
2) Area 1,2,3 ARE modality specific (columns for light touch vs. deep pressure) |
|
|
Term
| What are the activities of Pyramidal tract neurons during motor behavior? |
|
Definition
1) Send commands for movement
2) Flex/Extensor specific (set of functional muscles)
3) Encode amount of Force required for movement (firing rate)
4) Increase complexity, increase motor pool size
5) Small accurate movements require increased firing rates. |
|
|
Term
| What is Apraxia and how is it caused? |
|
Definition
Inability to perform skilled voluntary movements in absence of paralysis or severe sensory loss.
Damage to connections between Supplementary Motor/Pre-Motor cortices and Posterior Parietal Cortex. |
|
|
Term
| How does cortical control of antagonist muscle inhibition relate to the muscle spindle reflex? |
|
Definition
Just prior to contracting agonist muscles, cortex sends fast IPSP to antagonist and utilizes the same 1a afferent cells for continued inhibition during movement.
In the spinal chord, this is called Renshaw cell inhibition and involves glycine release. |
|
|
Term
| What are the 6 Eye muscles, their innervation and their preferred movements? |
|
Definition
1) LR (temporal)- VI- Ipsilateral
2) MR (nasal), IR (down when eyes are temporal), IO (up when eyes are nasal)- III- Ipsilateral
3) SR (up when eyes are temporal)- III- Contralateral
4) SO (down when eyes are nasal)- IV- Contralateral |
|
|
Term
| What are the 5 types of ocular movements? |
|
Definition
1) Saccade
2) Smooth pursuit (visual input required)
3) VOR
4) OKR
5) Vergence |
|
|
Term
What ocular deficits are caused by lesions in the Pons to
1) Left PPRF
2) Left MLF |
|
Definition
1) Slow saccade to left, because pph path is in tact, but direct path is not.
**Remember, PPRF projects to ipsilateral Vi nucleus (burst) and pph (tonic) and is important for saccadic movement**
2) Internuclear Opthalmoplegia
**Left MLF carries projections from right VI nucleus in pons to left III nucleus in Mesencephalon. The left eye cannot turn right with the right eye when the head turns to the left, and the right eye exhibits nystagmus** |
|
|
Term
| What ocular deficits are caused by lesions in the Medulla? |
|
Definition
1) Upbeat Nystagmus (integrator)
2) VOR asymmetry (gain control)
3) Abnormal smooth pursuit |
|
|
Term
| What is the primary difference between the neural control of Saccades and the VOR? |
|
Definition
1) Direct pathway of Saccades involves ipsilateral PPRF in pons
2) Direct pathway of VOR involves contralateral vestibular nucleus
** Both have indirect path involving pph in medulla |
|
|
Term
| How might a lesion to the Frontal Eyes Fields affect ocular movements? |
|
Definition
Directional information from the MST/V5 in the parietal lobe will not be able to get to the ocular muscles.
Remember the path.
Retina...LGN...Striate....MST/V5.....FEF...Pontine nuclei...Cerebellum...Vestibular N and PPRF....CN III...Muscles
** Superior Colliculus is also involved!** |
|
|
Term
| With age, the VOR often becomes "out of synch." How does the CNS accommodate for this? |
|
Definition
Gain decreases because eyes are slower than visual world (<1).
1) Cerebellum gets information from Vestibular Canal via mossy fibers (what is the head doing?) and from the Eyes via climbing fibers (what are the eyes doing).
2) Sends corrective signal to Vestibular N via Purkinje fibers to correct input sent to VI and adjust eye movement speed. |
|
|
Term
| How might a partial lesion to the left VI nucleus influence ocular movements for Saccades? |
|
Definition
You are messing with both the direct and indirect pathways here, so you get "choppy, ineffective movement"
1) PPRF is less effective at sending to signals to VI and III (via MLF)
2) pph is less effective at keeping the eyes in place after they move. |
|
|
Term
| Why does a lesion the left vestibular apparatus cause a VOR to the right when the head is static? |
|
Definition
1) The right vestibular n. is all that is active, so the brain "thinks" the head is moving to the right.
2) Rightward head movement excites contralateral VI nucleus, which projects to the left LR and the right MR (via MLF).
3) You get left "slow wave" with right "fast-phase." |
|
|
Term
| Why does ALS present with both UMN and LMN signs? |
|
Definition
1) Degeneration of neurons in Anterior Horn cause atrophy because of denervation of skeletal muscle
2) Degeneration of descending corticospinal tracts lead to UMN signs including hyper-reflexia, Present babinski and increased tone. |
|
|
Term
| How does axonal degeneration occur in peripheral nerves? |
|
Definition
Wallerian degeneration
**can occur in sensory neurons and cause neurogenic pain
1) Begins distally and proceeds proximally
2) Causes secondary disruption of myelin into balls called "Ovoids"
3) Leads to denervation which causes weakness, atrophy and loss of reflexes. |
|
|
Term
| How can you tell between Axonal Polyneuropathies (diabetes, alcoholism) and Demyelinating Neuropathies (MS, Guillain Barre)? |
|
Definition
CONFIRM WITH NERVE CONDUCTION
1) Axonal Neuropathy present with initial DISTAL sensory loss, weakness, hypo-reflexia and atrophy (EMG amplitudes are low, diffusely (less summed AP))
2) Demyelinating diseases are "segmental" and present more diffusely (Dispersed waveforms with evidence of slowed conduction on EMG) |
|
|
Term
| What is the cause of Myasthenia gravis and how is it treated? |
|
Definition
Look at eyes, face, swallowing and jaw
1) Post-synaptic, autoimmune NMJ disease, where antibodies attack AchR, leading to complement-mediated destruction of receptors.
2) Treat with AChE inhibitors and immunosuppression. |
|
|
Term
| What is the cause of Lambert-Eaton Myasthenic Syndrome (LEMS) and how is it treated? |
|
Definition
Associated with small-cell cancers
1) Pre-synaptic, autoimmune disease of NMJ, where antibodies attack VG-Ca channels, disrupting active zones and causing similar symptoms to Myasthenia gravis.
Presents with hyporeflexia and dry mouth, and you see low motor amp on EMG, due to low EPP, and marked increase in amplitude after excercise.
2) Treat with AchE inhibitors, immunosuppression and 3,4 diaminopyrodine (K-channel blocker that augments calcium release) |
|
|
Term
| How do inherited muscular dystrophies develop? |
|
Definition
Mutations in Dytrophin, which is a structural protein that links Actin to Sarcolema membrane in muscle, causes abnormal muscle contraction
Confirm with a biopsy. |
|
|
Term
A patient presents with proximal muscle weakness of limbs and neck flexors.
You detect no atrophy and the patient has normal sensation and reflexes.
You order a CK and EMG.
Why do you order these tests and what do you think this is? |
|
Definition
Proximal muscle weakness, lack of atrophy and in-tact sensory/reflexes (these may be lost as disease progresses) suggests there is an issue with the muscle itself.
1) CK (MOST COMMON) will be elevated in inflammatory, hypothyroid, dystrophic and metabolic myopathies.
2) Motor unit potentials (MUPs) will show decreased amplitudes in necrosis (fibrillations from disconnection, but NOT fasciculations at rest)
** If you see fasciulations, it is neurogenic in anterior horn or motor neuron** |
|
|
Term
| What are the 3 types of inherited vs. acquired myopathies? |
|
Definition
Acquired
1) Inflammatory (Polymyositis, Dermatomyositis)
2) Endocrine (Thyroid)
3) Toxic (Steroids)
Inherited
1) MD (Becker and Duchenne)
2) Metabolic (Mitochondrial, Glycogen, Lipid)
3) Congenital (Central Core) |
|
|
Term
A patient presents with fatiguable muscle weakness and ocular symptoms.
What is going on? |
|
Definition
| Ocular could be NMJ or myopathy, but fatiguable weakness is characteristic of NMJ. |
|
|
Term
| How can you distinguish M. gravis from LEMS? |
|
Definition
| LEMS (pre-synaptic calcium issue) presents with hyporeflexia and dry mouth |
|
|
Term
A patient presents with muscle atrophy, hyporeflexia and visible fasciculations.
What do you think is going on? |
|
Definition
| Atrophy and Fasciculations are probably an Anterior Horn Cell disease (i.e. ALS), but could be a peripheral nerve disease or LEMS (both present with hyporeflexia) |
|
|
Term
| How does sensory transduction differ between the auditory and vestibular systems? |
|
Definition
1) Vestibular apparatus has hair cells inside of ampulla embedded within cupula of crista organ
- Hair cells have Kinocilium and exhibit "resting discharge"
2) Auditory system has hair cells within cochlea with bases in basilar membrane and stereocilia contacting tectorial membrane
- Cells do not have Kinocilium and do not exhibit "resting discharge" |
|
|
Term
| How do the semicircular canals of the vestibular system measure angular acceleration? |
|
Definition
Ex) turn head to left, fluid in left horizontal canal moves right and deflects kilocilium towards utricle, leading to depolarization. The right horizontal canal experiences the opposite.
1) Horizontal canal has Kinocilia pointing towards the utricle and away from the central canal, and are excited with motion is towards Utricle.
2) Vertical canals have kinocilia pointing away from the utricle and towards the central canal and are excited when motion is away from Utricle. |
|
|
Term
| How do the otolith organs differ from the semicircular canals? |
|
Definition
1) Canals measure angular acceleration, while Otolith organs measure Static position of head in space and linear acceleration.
2) Stereocilia of O-organs are embedded in otolithic membrane (containing otoconia crystals) that has higher specific gravity than surrounding fluid. These hair cells exist in all DIFFERENT orientations.
- Stereocilia of canals are embedded in cupula of cristae organ and are all oriented in the same direction. |
|
|
Term
| How do the otolith organs calculate linear acceleration? |
|
Definition
| Hair cells in macula of Utricle (horizontal) and Saccula (Vertical) respond to movements of head in space |
|
|
Term
| What are the 6 major projections of the 4 vestibular nuclei? |
|
Definition
1) Bilateral interconnections
2) Cerebellum (fastigial/vermis and flocculus)
3) CN III, IV and VI
4) Spinal
5) Cortex (S1 and SII)
6) Brainstem (resp and circulation) |
|
|
Term
| How is vestibular caloric testing used clinically? |
|
Definition
Quick phase: COWS (Cold Opposite, Warm Same)
1) Warm water causes fluid to rotate towards ampulla, stimulating ipsilateral labryinth (contralateral slow phase and ipsilateral fast-phase)
2) Cold water is opposite (slow phase toward stimulation and fast-phase away). |
|
|
Term
| What extra-vestibular inputs do the 4 vestibular nuclei in the pons/medulla receive? |
|
Definition
| Many from muscle spindles of neck to coordinate neck/head movement. |
|
|
Term
| What is the functional anatomy of the cerebellum (input and output) |
|
Definition
1) Spinocerebellum= Vermis + Lateral Zone of Anterior/Posterior Lobes
- Receives spinal chord input through inferior peduncle
2) Cerebrocerebellum= Lateral zone of Anterior/Posterior lobe
- Receives input from from cortex via middle cerebellar peduncle
3) Vestibulocerebellum= flocculus + uvula + tonsil
- projects to vestibular nuclei |
|
|
Term
| Where do each of the 4 functional zones of the cerebellum project? |
|
Definition
1) Vermis- Fastigial (medial motor execution)
2) Lateral Zone- Nucleus interpositus (Globose + Emboliform) (lateral motor execution)
**1 and 2 are derived from Spinocerebellum
3) Lateral zone (cerebrocerebellum)- Dentate (motor planning)
4) Flocculonodular- Vestibular nuclei in pons/medulla (balance & eye movements) |
|
|
Term
| What is the difference between climbing and mossy fibers as they relate to a generic Cerebellar circuit? |
|
Definition
Afferents indirectly reach deep cerebellar nuclei through Purkinje fibers by first traveling via Mossy (through inhibitory interneurons) and Climbing fibers (from ION directly to Purkinje).
1) Mossy fibers indirectly inhibit Purkinje fibers, thereby de-inhiibiting deep nuclei (INCREASE OUTPUT)
2) Climbing fibers directly excite Purkinje fibers, thereby inhibiting deep nuclei (DECREASE OUTPUT)
** Remember, some afferents directly activate deep nuclei without passing through deep nuclei ** |
|
|
Term
| What are the major functions of each of the 4 deep cerebellar nuclei? |
|
Definition
All project out of cerebellum via Superior Cerebellar Peduncle towards to the thalamus
1) Fastigial (medial/proximal motor)- also projects via inferior peduncle to RF
2) Nucleus interpositus (lateral/distal motor)
3) Dentate (motor planning)
4) Vestibular (balance and eye movements)- also projects via inferior peduncle to vestibular nuclei. |
|
|
Term
| What is the only cerebellar input to produce contralateral deficits? |
|
Definition
| ION, which provides climbing fiber afferents via the inferior peduncle that directly activate Purkinje cells to ultimately inhibit the output of deep cerebellar nuclei. |
|
|
Term
| What is the basic bloods supply of the Cerebellum and the clinical consequences to each of the supplying arteries? |
|
Definition
1) PICA- inferior cerebellum (Lateral Medullary Syndrome)
2) AICA- Flocculus (Truncal ataxia, VOR gain issues, can't compensate for vestibular damage)
3) SCA- Superior cerebellum and deep cerebellar nuclei (issues from last of fastigial, nucleus interpolis and dentate) |
|
|
Term
A patient presents with a staggered wide gate and drifting while standing.
They complain that when they put on their bifocals, they feel quite dizzy.
What is going on and what else are you worried about? |
|
Definition
Flocculonodular Lobe damage (perhaps through stroke to AICA).
This is truncal ataxia and inability to adjust VOR gain.
This patient will not be able to compensate for vestibular apparatus damage, so they should be careful! |
|
|
Term
A patient presents with a positive Romberg and an abnormal "finger to nose" test.
What could be going on? |
|
Definition
truncal and appendicular ataxia appear together with damage to Spinocerebellum (vermis + intermediate zone of anterior and posterior lobes). This can arise from SCA infarction, potentially.
The Vermis and Intermediate zones project to the Fastigial and Nucleus interpolis, respectively, influencing motor control of proximal (truncal ataxia) and distal (finger-nose) musculature. |
|
|
Term
| What are the 6 classic sings of Cerebrocerebellum damage? |
|
Definition
Remember, the Cerebrocerebellum is synonomous with the lateral cerebellum, which projects Purkinje fibers to the dentate nucleus, which is critical for motor planning.
3D2H1I
1) Dysmetria (judging distance), Dysdiadochokinesia (rapid, alternating), Dyssynergia (chopping movements)
2) Hyotonia and Hyporeflexia ipsilaterally
3) Intentional tremor |
|
|
Term
| What are the major causes of Neonatal Meningitis vs. Child/Adult? |
|
Definition
1) Neonatal= Listeria, N. meningiditis, S. pyogenes
2) Child/Adult= N. meningiditis, S. pneumonia, Listeria, H. influenzae (poorer nations)
- TB (PCR of CSF), Syphillis, Lyme |
|
|
Term
| How does TB associated meningitis present differently then other forms? |
|
Definition
Brainstem (cranial nerve) involvement and decreased glucose with increased protein compared to other etiologies
Also increased ICP (seen elsewhere) |
|
|
Term
| How does Syphilis associated meningitis present differently then other forms? |
|
Definition
1) Asymptomatic CNS involvement, followed by meningovascular involvement and/or low- grade meningitis (multi-focal arteries)
2) Sometimes progresses 1-2 decades later to tabes dorsalis
3) Visual and Hearing deficits in HIV patients with neurosyphilis. |
|
|
Term
| How does Lyme-associated meningitis present differently then other forms? |
|
Definition
3 stages
1) Maculopapular rash
2) Cranial nerve palsies secondary to inflammation of roots in subarachnoid space
3) True encephalitis. |
|
|
Term
| How does root of entry help cue you into the type of pathogen causing a brain abscess? |
|
Definition
1) There are those that enter frontal lobe directly through sinuses (S. pneumo or H. influenze), or temporal lobe via mastoiditis (S. pnuemo and Pseudomonas)
2) If they enter through blood, they end up in grey-white junction. |
|
|
Term
| What are the major signs to look for in a NMJ issue? |
|
Definition
1) Weakness with sustained exertion
2) Gets worse as day progresses
If 1 and 2 are false, but 3 is true, think Myopathy
3) No sensory,reflexes, bulk or fasciculation issues |
|
|
Term
| A patient presents with persisting contraction of after handgrip. What is going on? |
|
Definition
This is Myotonia and caused by impaired electrical properties of muscle of muscle membrane.
Seen specifically in Myopathy. |
|
|
Term
A patient presents with lower, left facial weakness, lower arm and body weakness and numbness, and tongue deviating to left.
What is going on? |
|
Definition
RIght internal capsule, posterior limb (all same side, think IC)
Lower half of face suggests supranuclear lesion (UMN) and left body/leg suggests Corticospinal tract. |
|
|
Term
| What structures normally control elevation (or closure) of the eyelid? |
|
Definition
Elevation
1) Levator palbebrae- CN III, CNIII nucleus
2) Superior tarsal muscle- Superior Cervical Ganglion (symp)
3) Obicularis oculi- facial nerve- facial motor nucleus. |
|
|
Term
A patient cannot constrict their pupil.
What is the pathway involved in this abnormality? |
|
Definition
Parasympathetic
1) Retina...Nerve...Chiasm...Tract
2) Pre-tectal nucleus...Edinger-Westphal (CN III)
3) CN III...CIliary ganglion...Ipsilateral constrictor of iris |
|
|
Term
A patient cannot dilate their pupil.
What is the pathway involved in this abnormality? |
|
Definition
Sympathetic
1) Pre-ganglionics in Thoracic intermediolateral cell column synapse in synpathetic chain ganglion.
2) Post-ganglionics project to ipsilateral pupillary dilator (radial) muscle of iris |
|
|
Term
| What valuable information can you gleam from whether a ptosis is partial or complete? |
|
Definition
Complete usually indicates issue with Levator Palpebrae, which suggests CN III issue.
Partial usually indicates issue with Superior Tarsal, which suggests sympathetic issue.
**Closing eyelid is Obicularis oculi (CN VII) |
|
|
Term
A patient presents with stiff neck and you are worried about Meningitis.
What causes this pain in Meningitis? |
|
Definition
| Blood in sub-arachnoid space (usually from bursted aneurism) that activates pain receptors in meninges. |
|
|
Term
| Why is the spinothalamic system spared in Paramedian pontine syndrome? |
|
Definition
| The paramedian branches of the Basilar artery supply the medial pontine nuclei (VI, VII, Corticospinal, Medial Lemniscus), but not the more lateral, spinothalamic tract. |
|
|
