1
Q
Red flags for headache?
A
- Age > 50 years
- Worst of life
- First of life
- “Thunderclap” onset
- Marked change in pattern
- Unusual associated features (blindness, diplopia, confusion, weakness)
- Meningeal signs
- Lack of response to abortive medications
- Recent malignancy, head trauma or seizures
- Unexplained fever
- Blood pressure greater than 180/115
- Persistent or unexplained vomiting
- Focal abnormalities
2
Q
Pain sensitive structures in head?
A
- Pain sensitive structures: skin, blood vessels, muscles, venous sinuses, pain fibers of CN5/7/9/10, and parts of dura mater
3
Q
What nerves supply sensory to head and neck?
A
- Pain of head
- Trigeminal nerves (V1-3) supply sensory information from the anterior head, C2 supplies the posterior head, and C3 supplies the neck
4
Q
Dx of HA?
A
- Diagnosis of headaches
- HPI, PE, imaging, LP, blood studies, referral
5
Q
Migraine pathophys?
A
- Migraines
- Pathophysiology: neural dysfunction → vasodilation of cerebral blood vessels → irritation of trigeminal nerve ending → release of vasoactive peptides (Substance P and CGRP) → further vasodilation → neurogenic inflammation → pain and pulses sent through trigeminal nerve → trigeminal nucleus caudalis in brainstem → spinothalamic pathway → thalamus → sensory cortex
6
Q
Triggers of migraine? Signs of migraine (know mnemonic).
Characteristics of aura associated with migraine
A
- Triggers: skipping meals/diet change, diet triggers, sleep too much/little, stress, hormones
- Signs (POUND): Pulsating pain, One day duration, Unilateral, Nausea/vomiting, Disabling + phonophobia/photophobia and possible aura
- Aura (visual, sensory, or speech): gradual progression over 5-60 minutes, unilateral, accompanied by headache within 1 hour of aura
7
Q
Treatment of migraine (Acute and prophylaxis). there are a lot. Know basic MOA
A
- Treatment:
- Acute: NSAIDs, triptans, dihydroergotamine, steroids, valproate (MOA : GABA agonist), monoclonal antibodies (anti-CGRP)
- Triptan MOA: 5HT1D (trigeminal nerve ending) and 5HT1B (cranial blood vessel) agonists
- Prophylaxis: lifestyle changes (sleep, exercise, diet), beta blockers, calcium channel blockers, amitriptyline (MOA: inhibits reuptake of NorEpi/5-HT), topiramate (MOA: Ca+ blocker), valproate, gabapentin (MOA: Ca blocker and GABA agonist)
- Acute: NSAIDs, triptans, dihydroergotamine, steroids, valproate (MOA : GABA agonist), monoclonal antibodies (anti-CGRP)
8
Q
Signs, tx (acute and prophylaxis) of cluster HA
A
- Cluster headaches (i.e. Trigeminal autonomic cephalgias)
- Signs: repetitive brief unilateral headaches, severe preorbital pain with lacrimation, rhinorrhea, +/- Horner’s syndrome, lasts 15 min to 3 hrs (repetitive)
- Treatment:
- Acute: sumatriptan, O2
- Prophylaxis: verapamil
9
Q
For trigeminal neuralgia: signs and tx (3)
A
- Trigeminal neuralgia
- Signs: repetitive, severe unilateral shooting pain in the distribution of CN V division(s), lasts <1 min
- Other cranial neuropathies: glossopharyngeal n, nervus intermedius n, occipital n
- Treatment: carbamazepine (first-line), Baclofen, gabapentin
- Signs: repetitive, severe unilateral shooting pain in the distribution of CN V division(s), lasts <1 min
10
Q
For tension headaches: signs, tx (acute and chronic)
A
- Tension headaches
- Signs: bilateral steady pain lasting > 30 min; constant for 4-6 hours
- No photophobia/phonophobia, no aura
- Treatment
- Acute: analgesics (NSAIDs, acetaminophen)
- Chronic: amitriptyline
- Signs: bilateral steady pain lasting > 30 min; constant for 4-6 hours
11
Q
For secondary HA: etiologies, and signs of traumatic HA?
A
- Secondary headaches
- Etiologies: trauma, vascular, intracranial nonvascular, substance, infection, homeostasis, HEENT, psychiatric
- Signs for traumatic headache: injury to head, HA within 7 days, HA persists for >3 months after injury
12
Q
Define epilepsy. What is the operational diagnosis?
A
- Epilepsy: neurological disorder associated with abnormal electricity in the brain marked by recurrent episodes of central disturbance, LOC, and convulsions
- Operational diagnosis: two unprovoked seizures >24 hours apart or 1 unprovoked seizure w/ underlying brain/metabolic abnormality; EEG
13
Q
Define seizure
A
- Seizure: transient disturbance in cerebral dysfunction due to paroxysmal neuronal discharge (can be a result of a disease unrelated to epilepsy)
14
Q
Define a partial seizure. What are the 2 types (new and old names)? What are the clinical presentations (list by lobe they present from)
A
- Partial (focal or localized): affects the single area of the brain (common mediotemporal lobe), can be preceded seizure aura, and can secondarily generalize
- Types: Simple/aware (conscious), Complex/impaired (impaired consciousness)
- Clinical presentation (slow onset and recovery):
- Temporal lobe: automatisms – repetitive motions, altered speech, hallucinations
- Frontal lobe: motor activity, posturing, can occur in clusters
- Parietal lobe: sensory changes
- Occipital lobe: visual changes
15
Q
Describe generlaized seizures. List the 5 types (know different names if applicable)
A
- Generalized: affects the brain diffusely and bilaterally
- Tonic-clonic (grand-mal)
- Tonic
- Absence (petite-mal)
- Atonic
- Myoclonic
*
16
Q
For tonic-clonic, whats another name for it?
What is the clinical presentation (age and length)?
What are the phases with characteristics of each phase?
A
- Tonic-clonic (grand-mal)
- Clinical presentation: any age, lasts 1-3 minutes
- Phases: premonition → pre tonic-clonic (brief myoclonus) → tonic (epileptic cry, stiffening) → clonic (incontinence, rhythmic jerking fast to slow) → postictal (unresponsive or lethargic)
17
Q
What is the clinical presentation of a tonic seizure?
A
- Tonic
- Clinical presentation: stiffening
18
Q
For absence seizure, know a different name. Know clinical presentation (age, length, sx), and know dx
A
- Absence (petite-mal)
- Clinical presentation: children/adolescents, lasts <30 seconds, sudden LOC (blank stare, no-post-ictal confusion), minimal motor activity
- Dx: EEG (3 Hz spike wave)
19
Q
What is the clinical presentation for atonic seizure
A
- Atonic
- Clinical presentation: drop seizures (falls to floor); mistaken for fainting
20
Q
For myoclonic seizure: what is the clinical presentation (age, length, sx)? It is a key feature of what syndrome?
A
- Myoclonic
- Clinical presentation: all ages, lasts 1-5 seconds, lightning fast jerks of head/arms/legs (aka twitches), can occur in clusters
- Key feature of Juvenile Myoclonic Epilepsy (JME)
21
Q
What is the best way to diagnose seizures?
In this modality, what would normal, focal, and generalized look like?
A
- Diagnosis of seizures:
- Electroencephalogram (EEG): measures electrical brain activity to detect abnormal discharges between/during seizures
- Normal: consistent alpha waves without any spikes
- Focal: consistent alpha waves with focal spikes in some leads
- Generalized: spikes for a prolonged period in all leads
- Electroencephalogram (EEG): measures electrical brain activity to detect abnormal discharges between/during seizures
22
Q
What are the various etiologies of seizures?
A
- Etiology of seizures: structural (i.e. brain damage, malformation, vascular), infectious (i.e. neurocysticerosis), metabolic (i.e. pyridoxine-dependent), immune (i.e. autoimmune disease), genetic (aka idiopathic), unknown
- Idiopathic is most common
23
Q
What are the goals of antiseizure therapy?
A
- Complete seizure control, no SE,
24
Q
Principles of starting and stopping treatment for epilepsy
A
- Starting meds:
- Requires diagnosis of epilepsy + consideration of lifestyle effects and severity of seizures
- Stopping meds
- Standard practice: treatment until two years seizure-free → consider tapering
25
**Factors to consider in choosing a medication**
* Seizure type, side effect profile, related meds, dosing forms, dosing intervals, insurance
26
**Principles of side effects of medications**
* Dose Related
* Sedation, lethargy
* Ataxia and unsteadiness
* Idiosyncratic
* Rash and Stevens-Johnson Syndrome
* Hepatic toxicity
* Bone Marrow suppression
* Genetic
* HLA-B\*15:02 association with Stevens-Johnson in those of Han Chinese decent
* Single nucleotide polymorphism – CYP2C9\* and phenytoin-induced cutaneous reaction
* Many others SEs likely genetically related
* Long term
* Interference with Vitamin D and bone metabolism
* Effect on the brain and cognition
* Teratogenetic: major congenital malformations
* Myelomeningocele, cleft lip and palate
* Drugs with high teratogenic effect: valproate, topiramate, phenytoin
27
What are some other treatments for epilepsy?
* Steroids and Adrenocorticotropin hormone (ACTH)
* Dietary treatment – Ketogenic diet
* Vagal Nerve Stimulation
* Cannabis – Cannabidiol
* Other alternative therapies, e.g. essential oils, such as frankincense (proof is lacking but plenty of websites)
28
List non epileptic uses of antiepileptics
* Mood and Anxiety Disorders: Lamotrigine, Valproate, Carbamazepine, Topiramate, Benzodiazepines
* Neuropathic Sensory Disorders: Carbamazepine, Gabapentin, Pregabalin, Lamotrigine, Levetiracetam
* Headache: Topiramate, Valproate, Gabapentin
* Tic Disorders: Topiramate
29
Name the 3 types of drugs
30
What are the 4 drugs?
31
What are the 5 drugs?
32
Define white matter disease and demyelination and dysmyelination?
* Definition of white matter disease: pathology of myelinated axons and oligodenodrocytes
* Demyelination: breakdown of myelin (lipid-based)
* Dysmyelination: failure of formation of normal myelin
33
Clinical presentation of central myelin conditions
* Clinical Presentation
* Symptoms: spasticity, hyperreflexia (Babinksi sign), ataxia, optic atrophy
* Different from gray matter disease: seizures, dementia, retinal changes
34
What are the imaging modalities used to dx central myelin conditions?
* Imaging
* MRI (T2 hypersensitivity and FLAIR show hypoechoic lesions)
35
What are pathologic features noted in central myelin conditions? What are 4 acquire disease types of central myelin disease (give examples of each)?
* Pathologic Features
* Loss of myelin staining seen on Luxol Fast Blue (lack of blue)
* Acquired disease types:
* Toxic (i.e. central pontine myelinolysis), Nutrition (i.e. B12 deficiency subacute combined degeneration), Infectious (i.e. syphilis, HIV, PML), Immune-mediated (i.e. MS)
36
For Adrenoleukodystrophy (ALD)
* Pathophys
* Acquired/genetic? If genetic, what gene/mutation?
* Clinical presentation
* Tx
* Adrenoleukodystrophy (ALD)
* Genetics: x-linked recessive; carriers may have symptoms
* Pathophysiology: defect in ATPase binding cassette protein (ABCD1) → defect in peroxisomal beta oxidation → disruption of metabolism of very long chain fatty acids → excessive buildup of myelin, adrenal gland, and Leydig cells of testes
* Clinical presentation: neuro sx (progressive), adrenal insufficiency sx (hyperpigmentation, hypoglycemia, dehydrated)
* Childhood cerebral ALD: onset between 4-10 years old, often progresses rapidly to vegetative state with adrenal insufficiency
* Treatment: adrenal enzyme replacement (corticosteroid), hematopoietic stem cell therapy, gene therapy
37
For Metachromatic Leukodystrophy
* Pathophys
* Acquired/genetic? If genetic, what gene/mutation?
* Clinical presentation
* Metachromatic Leukodystrophy
* Genetics: autosomal recessive
* Pathophysiology: deficiency of arylsulfatase A cells → buildup of sulfatides → impaired production and destruction of myelin sheath
* Clinical presentation: central and peripheral demyelination with dementia and ataxia
38
For Krabbe disease
* Pathophys
* Acquired/genetic? If genetic, what gene/mutation?
* Clinical presentation
* Dx
* Krabbe disease (Krabbe Globoid Cell)
* Genetics: autosomal recessive
* Pathophysiology (lysosomal storage disease): deficiency of galactocerberoside beta-galactosidase → accumulation of galactocerbrosides and psychosine in macrophages →destruction of myelin sheath
* Clinical presentation: peripheral neuropathy, developmental delay, optic neuropathy
* Diagnosis: globoid cells
39
For Charcot-Marie Tooth
* Description
* Acquired/genetic? If genetic, what gene/mutation?
* Clinical presentation
* Charcot-Marie Tooth (hereditary motor and sensory neuropathy)
* Genetics: autosomal dominant
* Description: group of progressive hereditary nerve disorders that result in dysfunction of _peripheral_ nerves and the myelin sheath
* Clinical presentation: foot deformities (pes cavus), lower extremity weakness (footdrop), sensory deficits
40
For Progressive Multifocal Leukoencephalopathy
* Etiology
* Risk Factors
* Acquired/genetic? If genetic, what gene/mutation?
* Pathophys?
* Clinical presentation
* Progressive Multifocal Leukoencephalopathy (ACQUIRED)
* Etiology: JC virus infection of oligodendrocytes
* Risk Factors: AIDS, leukemia, drugs (Natalizumab, rituximab)
* Pathophysiology: immunosuppression → reactivation of latent JC virus → destruction of oligodendrocytes → demyelination
* Clinical presentation: rapid onset of neuro signs (visual loss, weakness, dementia), death
41
For acute disseminated encephalomyelitis:
* Acquired/genetic?
* Pathophys?
* Clinical presentation
* Acute disseminated (post-infectious) encephalomyelitis (ACQUIRED)
* Pathophysiology: infection/vaccination à multi-focal inflammation and demyelination
* Clinical presentation: rapid onset neurological symptoms and AMS
42
What is the pathophys of HIV?
Discuss primary HIV infection of CNS as well
* Pathophysiology: HIV attaches to CD4 on T-cells → virus core enters cell → reverse transcriptase +ssRNA → dsDNA → integrase inserts viral dsDNA into host DNA → mRNA is transcribed and translated by host machinery → new HIV proteins → new HIV virion is released from cell
* Primary HIV infection can lead to opportunistic brain infections by other organisms due to immunocompromised state (listed below)
* Primary HIV infection of the CNS: HIV → enters CNS via infected monocytes that cross BBB → release of cytokines/chemokines → inflammation → invasive encephalitis → HIV associated dementia
43
* For HIV
* What is the pathology (Histo/MRI)
* Signs/sx (Acute/chronic)
* Tx (MOA and SE)
* Pathology:
* Histological differences: mononuclear cells and astrocyte infiltration → pale pink myelin
* Normal: darker pink with many cells visible
* MRI: atrophy of the brain cortices and swelling of the ventricles
* Signs/sx:
* Acute: encephalitis, Bell’s palsy, transverse myelitis, demyelination polyneuropathy, vacuolar myelopathy (similar to B12 deficiency)
* Chronic: asymptomatic/mild neurocognitive disorder, HIV associated dementia
* Tx: antiretroviral therapy (ART) has decreased mortality
* ART has poor penetration of BBB → chronic sx persist
* SE: ART is neurotoxic, Neruo IRIS (immune system recovers → heightened response to opportunistic infections → inflammation)
* Neuro IRIS risk factor: low CD4 count
44
For **Progressive multifocal leukoencephalopathy (PML)**
* Pathogen
* Pathophys
* Signs/sx
* Dx
* Pathology
* Prognosis
* Tx
**Progressive multifocal leukoencephalopathy (PML)**
* Pathogen: JC virus (polyomairus), usually maintained in latent state
* Pathophysiology: latent state of JC virus → reactivation after immunosuppression → infection of oligodendroglia → demyelination
* Signs/sx: progressive neurologic decline
* Diagnosis: MRI (multifocal areas of high signal in white matter). Immunohistochemistry
* Pathology (gross): punched out white matter lesions with clear margins
* Prognosis: often fatal
* Treatment: antiretroviral treatment for HIV
45
For **Primary CNS Lymphoma**
* Pathogen
* Signs/sx
* Dx
* Pathology
* Tx
**Primary CNS Lymphoma**
* Pathogen: associated with Epstein-Barr virus (+HIV) infection
* Signs/sx: AMS, focal neuro sx, +/- seizures, fever, night sweats, weight loss
* Diagnosis: brain biopsy
* Pathology:
* MRI: ring enhancing lesions post Gd administration
* Pathology: lymphoid cells with predominantly with B-cell markers
* Treatment: radiation therapy, chemotherapy, steroids
46
For **Toxoplamosa encephalitis**:
* Pathogen
* Signs/sx
* Dx (imaging, other)
* Pathology
* Tx
**Toxoplamosa encephalitis**
* Pathogen: T. gondii (intracellular parasite)
* Acquired from oocysts from cat feces or bradyzoites from undercooked meat
* Signs/sx: HA, fever, confusion, and seizure (minimal sx in immunocompetent patient)
* Diagnosis:
* Imaging: multifocal ring enhancing brain abscesses
* Serum serologies, CSF PCR
* Pathology: cysts that can rupture and release tachyzoites
* Treatment: antiparasitic agents and anti-retrovirals
47
For **Cytomegalovirus meningoencephalitis**:
* Description
* Signs/sx
* Dx
* Tx
**Cytomegalovirus meningoencephalitis**
* Description: acute diffuse necrotizing and demyelinating encepahlitis
* Signs/sx: polyradiculopathy, weakness, loss of DTRs, loss of bowel/bladder control, hemorrhagic retinopathy
* Diagnosis: CMV CSF PCR or viral culture of CSF
* Histology: necrosis, cytomegaly, and intranuclear inclusion (owl eyes)
* Treatment: ganciclovir, valganciclovir, foscarnet
48
For **Tuberculosis meningitis**:
* Pathogen
* Signs/sx
* Dx
**Tuberculosis meningitis**
* Pathogen: mycobacterium tuberculosis
* Signs/sx: basilar (affects base of brain) meningitis affecting CNs and hydrocephalus
* Dx: CT and MRI, CSF analysis, PCR
49
For **Cryptococcal meningitis**:
* Signs/sx
* Pathology
* Dx
* Tx
**Cryptococcal meningitis**
* Signs/sx: fever, HA, N/V
* Pathology: circular to ovoid with thick capsules with narrow-based budding yeasts
* Gross: can form cysts in the base of the brain
* Diagnosis: CSF analysis/cryptococcal antigen and India ink
* Treatment: Amphotericin B + fluconazole
* Prevention: fluconazole IF CD4 \< 100
50
For neurosyphilis:
* Pathogen
* Signs/sx
* Pathology
* Dx
* Tx
**Neurosyphilis**
* Pathogen: Treponema pallidum
* Signs/sx: asymptomatic, meningitis, strokes, transverse myelitis, chronic meningoencephalitis (paretic), tabes dorsalis
* Chronic meningoencephalitis: dementia, psychosis, and weakness
* Tabes dorsalis: progressive dorsal column dysfunction with pain
* Pathology (paretic presentation): thickened walls of small vessels and decreased number of neurons, and activated micrglia
* Diagnosis: serum tests (VDRL/RPR and FTA-ABS) and CSF tests (VDRL and PCR)
* Treatment: penicillin
51
* For meningitis
* Define
* Provide bacterial etiologies based on age group!
**Meningitis**
* Definition: infection of the leptomeningnes (subarachnoid and dura mater) and CSF
* Bacterial etiologies (in order of most common)
* 0-2 y/o: Group B Streptococcus, E. coli, Listeria monocytogenes
* 2-29 y/o: S. pneumoniae, N meningitidis (diplococci bacteria)
* 30-59 y/o: S. pneumoniae, N meningitidis, H. influenza (non-vaccinated)
* \>60 y/o: S. pneumoniae, Group B Streptococcus
52
For meningitis: pathophys, signs/sx, risk factors
* Pathophysiology:
* Pathogens enter respiratory tract → hematogenous dissemination → crosses BBB via cerebral capillaries/choroid plexus → infection of the meninges
* Other routes of infection: upper sinus infection (i.e. otitis media), traumatic fracture, osteomyelitis, myelomeningocele
* Signs/sx: N/V, HA, photophobia, seizures, nuchal rigidity, +meningeal signs, +/- fever, confusion
* Risk factors: nosocomial (ENT surgery, CSF leak), immunocompromised (AIDS, transplant, corticosteroid)
53
* For meningitis:
* Dx (any contraindications
* Tx (per age group)
* Diagnosis: LP
* CT indicated when: focal deficit, papilledema, new seizure, LOC, immunocompromised, known CNS lesions
* Contraindicated: patients w/ high ICP due to risk of herniation
* Treatment:
* Newborn: Ampicillin + gentamicin/cefotaxime
* 2 – 50 y/o: Vancomycin + ceftriaxone/cefotaxime
* \>50 y/o: Ampicillin + vancomycin + ceftriaxone/cefotaxime
* Dexamethasone is indicated in bacterial meningitis
54
For meningitis:
* Prevention
* Complications
* Prevention: H. influenza type B vaccine, pneumococcal meningitis vaccine, meningococcal meningitis vaccine
* Chemoprophylaxis (prophylactic treatment to those exposed to infection – i.e. daycare): required in N. meningitidis and H. influenzae
* Complications: cognitive impairment, cranial neuropathies, seizures, hydrocephalus, stroke, edema/herniation
55
What disease for each LP finding?
56
For brain abscess:
* definitions
* signs/sx
* risk factors
* dx
* List types
* Tx
**Brain Abscess**
* Definition: focal infection of the brain, specifically in parenchyma or subdural/epidural space
* Signs/sx: HA, mass effect. Fever, +/- N/V, +/- seizures, +/- papilledema
* Risk factors: bacterial endocarditis, pulmonary infection, R to L cardiac shunt
* Diagnosis: CT or MRI shows “ring-enhancing lesion(s)”, brain biopsy
* Types:
* Epidural abscesses
* Subdural abscesses
* Tx: Abx (vancomycin/naficillin + ceftriaxone/cefotaxime + metronidazole) + drainage
57
For epidural abscess: what are characteristics if it is in the brain vs spinal cord
* Epidural abscesses:
* Brain: localized, less serious, spreads from sinus
* Spinal cord: associated back pain, cord compression, very serious
58
For subdural abscess: etiology, signs/sx, complications
* Subdural abscesses:
* Etiology: aerobic bacteria (most common)
* Signs/sx: hemiparesis, altered consciousness, seizures, +/- papilledema, focal deficits, +/- speech impairment
* Complication: increased ICP → venous occlusion
59
For optic neuritis:
* Description
* Signs
* Diagnosis
* Ddx
**Optic Neuritis**
* Description: inflammation of the optic nerve
* Signs/sx: painful visual loss, decreased visual acuity, dyschromotopsia (reduced color perception)
* Diagnosis: blurring of optic disc on fundoscopic exam
* Pupillary response is defective in affected eye, MRI (optic nerve may be enhanced as it takes up contrast), slow visual evoked potentials in affected eye, optic coherence tomography (visualizes thickness of nerve)
* Ddx: MS (presenting symptom), Lyme, viruses, SLE, idiopathic
60
For multiple sclerosis:
* Description
* Epidemiology
* Pathophys
* Sign/sx
**Multiple Sclerosis (MS)**
* Description: autoimmune disorder that affects the CNS
* Epidemiology: women, young, northern latitudes (lack of Vit D)
* Genetics: HLA-DRB1
* Pathophysiology: antigen sensitization → T-cells cross BBB → T-cell attack oligodendroglia → immune cascade → release of cytokines (TNF-alpha, IFN-gamma, IL-2) → B-cell activation → IgG production
* In RRMS: oligodendroglia try to remyelinate axons → see acute attacks with stable periods in between
* T-regulatory cells down-regulate immune response
* Signs/sx: slow in onset and resolution, not localized in one area, worse in heat (Uhtoff’s), worse with neck flexion (L’hermitte Sign), numbness, weakness, vision, speech, swallowing, seziures,
* Charcot triad (SIN): scanning speed, intention tremor, and nystagmus
61
For multiple sclerosis:
* Types and how do they progress
* Types:
* Benign MS: no disability b/c return to normal between attacks
* Relapsing and remitting MS (RRMS): increasing disability after each spike of an acute attack
* Secondary progressive MS (SPMS): increasing disability after each spike of an acute attack → steady increase in disability with no acute attacks
* Primary progression MS (PPMS): steady increase in disability with no acute attacks
62
Multiple sclerosis diagnosis?
What needs to be ruled out?
* Diagnosis
* MRI: shows Dawson’s fingers perpendicular to ventricle
* CSF evaluation: protein (normal to elevated), IgG synthesis rate increased
* Oligoclonal bands are increased in only CSF (not serum)
* McDonald criteria: using clinical events and MRIs studies to show dissemination in space and time
* Rule out: sarcoidosis (ACE), Lyme disease (antigen studies), HIV (CD4), Thyroid (TSH), SLE (ANA), Sjogren’s (ANA, ssA, ssB), Syphillis (VDRL, RPR)
63
MS Tx: acute, 1st line meds, 2nd line, lifestyle changes, and symptomatic tx
**Multiple Sclerosis Treatment:**
* Acute: IV corticosteroids
* 1st line:
* Glatiramer acetate: decreases Th1 cells via Th reg cells
* IFN-beta: prevents T-cell migration
* Fingolimod: prevents T-cell migration to CNS by holding lymphocytes in lymph nodes
* Teriflunomide: decreased T-cell synthesis
* Dimethyl fumarate: decreases inflammatory response via activation of Nrf2 pathway
* 2nd line
* Natalizumab: binds integrin preventing T-cell migration
* Risk of PML
* Mitoxantrone: causes breakage in DNA → immunosuppression
* Lifestyle: no smoking, exercise, Vit D, biotin, low salt diet, probiotic, coffee
* Symptomatic treatment:
* Neurogenic bladder: catheter, muscarinic antagonist
* Spasticity: baclofen, GABA beta agonists
* Pain: TCAs, anticonvulsants
