NP
NephrologyKatie Connolly, Melanie Ostrekher and EliAa
Rennert-May, chapter editors Doreen Ezeife and Nigel Tan, associate
editors Steven Wong, EBM editor Dr. Ramesh Prasad, Dr. Martin
Sc:hreiber and Dr. Gemini Tanna, staff editorsBasic Anatomy Review
................... 2 Anatomy of the Kidney Renal Structure and
Function Renal Hemodynamics Differential Diagnoses of Common
Presentations . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Azotemia Proteinuria Hematuria Assessment of Renal Function
............. 6 Measurement of Renal Function Urinalysis Urine
Microscopy Urine Electrolytes Electrolyte Disorders. . . . . . . .
. . . . . . . . . . . . . 9 Sodium Homeostasis Hyponatremia
Hypernatremia Potassium Homeostasis Hypokalemia Hyperkalemia
Acid-Base Disorders .................... 16 Metabolic Acidosis
Metabolic Alkalosis Renal Failure .......................... 19
Presentation of Renal Failure Acute Kidney Injury (AKI)
................ 20 Approach to AKI Chronic Kidney Disease (CKD) .
21 Management of Chronic Kidney Disease Renal Replacement Therapy
............. 22 Dialysis Renal Transplantation Glomerular Disease
.................... 23 Terminology of Glomerular Changes
Presentation of Glomerular Disease Investigations for Glomerular
Disease Secondary Causes of Glomerular Disease Infections and
Glomerular Disease Tubulointerstitial Disease ............... 27
Tubulointerstitial Nephritis (TIN) Acute Tubular Necrosis (ATN)
Analgesic Nephropathies Vascular Diseases of the Kidney ..........
30 Large Vessel Disease Small Vessel Disease Systemic Diseases and
the Kidney ........ 32 Hypertension (HTN) Hypertensive
Nephrosclerosis Renovascular Hypertension Renal Parenchymal
Hypertension Multiple Myeloma Malignancy Diabetes and the Kidney
................ 34 Cystic Diseases of the Kidney ............ 36
Adult Polycystic Kidney Disease Medullary Sponge Kidney Autosomal
Recessive Polycystic Kidney Disease Common Medications .. 38
Landmark Nephrology Trials .. 39 References . . . . . . . . . . . .
. . . . . . . . . . . . . . . . 40
Toronto Notes 2011
Nephrology NPI
NPl Nephrology
1'oroDio
2011
Basic Anatomy ReviewAnatomy of the Kidney
Renal Structure and FunctionThe Nephron basic structural and
functional unit ofthe kidney, approximately I million per kidney 2
main components: glomerulus and attached renal tubule (Figure I)
direction of blood flow: afferent arteriole -+ glomerular
capillaries -+ efferent artuiale -+ vasa recta (the capil.laries
surrounding the tubules) -+renal venules
0
Osmatic diuratics liEzide diu191ics K+ Sparing
dianticso.-.lingII!Dolloop .alllonil
( ) L.oapdiul'ltics
0
Q
I1!1!
! :z:N1+K
i ;a
i
N1+-K- 2CI-
H,D -
l
I I Iz
2
Madula
0 [
Jli
I0
1. N1p1Jnm Compa1antsTlble 1. MaJor Fu1dons of the Kidneys1.
Willa EKrltiGn
Ghmarular fi1nl1ionTubailr secretion Tub.-r calllxllism Tubailr
tllaCI and Wllllr rubsGiptilll Tubaar Kseaetion Tub.-r HaecratiCII
HCO, synlheais ..:1 rBaa!ption Tubular Ca, Mg. P04
lnllspartElytlqail!lil pracb:lian lcorttxl Vitamin Ddvation
[25[0H)D 1,25(0HJDI Ranil praductian (JG applfiiUi)
(urea, Cl)
Eiu:mian of nitragnJUs prDib:ls of pratailrnelllbalism
Excretion af organic (!Ne) and Dfllllnic bases (Cr) llnllkdawn
end ucratian af drugs {..tDalicl, diul'llicll) end peplida hlmlanes
(mast pituillry harmCIIIIS, ilsUin.Clllllds vduma s1a1us and
osmolar balance Clllllds pllillssium cai!CI!nlnllian Al:id-basa
balance Al:id-basa balance .Min Ca. Ma-1'04 harnaastasis Calcium
hiDII!IISialis
Red lilad eel proU;Iian
Allin VIICUI.-ra&i&Wlcellllaldastlmle sacratian Allin
ECF Allin VIICUiar rnista1ceGlucose !llp!iY lllllintailed in
prnlanged staiYIIIion
....aod ............... Na IIKL18tian Ranil
praductianGluconeogereis tfmm lacbde, py!\MII8 end smila acids)
'IbroDlo Nota 2011
Buic Anatomy Review
Nephrology NP3
The Glomerulus site where blood constituents are filtered
through to the kidney tubules fur excretion or reabsorption
consistB of following cell types 1. capillary endotbelial cells and
podocytes support the glomerular basement membrane (GBM) and furm
the plasma filtration apparatus 2.mesangialcells have contractile
properties and produce YllSoad:i.ve substances to help control
blood flow 3. parietal epithelium covers the interior of Bowman's
capsule filtration occurs aaoss the GBM Into Bowman's space (Figure
2) filtration barrier: conaists ofcapillary endothelium, GBM.
podocyte filtration alit& particles are selectively filtered by
size (20 mmolJL) in the setting of acute renal failure: indicates
renal disease vs. pre-renal high urine Na (>40 mmolJL) in the
setting of hyponatremia: generally from causes such as diuretics,
tubular disease (e.g. Bartter's syndrome), SIADH additionally,
urine pH is useful to grossly assess renal acidification "low" pH (
100 cc,lhr, < 1DD mOsmiL) in lha sstting of hyponalr8mia is
u.uaUy thefi!$1: sign of dangerously rapid C01111Ction of serum
&Odium
... ' .-----------------. ,Conection of Na in hyponab8mia should
dlfinitlly known to t. 5.0 mEq!LApproach to Hyperkalemia 1.
emergency measures: obtain ECG, if life threatening begin treatment
inunediately 2. rule out factitious hyperkalemia; repeat blood test
3. hold exogenous K, and any K retaining medications 4. assess
potential causes of transcellular shift 5. estimate GFR (calculate
CrCl using Cockcroft-Gault) 6. if normal GFR, calculate TTKG =
(Uk/PJ4 weeks
Treatment1. preliminary measures pre-renal correct prerenal
factors: optimize volume status and cardiac performance, hold
ACEI/ARB renal exclude reversible renal causes: die nephrotoxic
drugs, treat infection, and optimize electrolytes post-renal
consider obstruction: structural (stones, strictures) vs.
functional (neuropathy) treat with Foley catheter, indwelling
bladder catheter, nephrostomy, stenting 2. treat complications
fluid overload NaCl restriction high dose loop diuretics
hyperkalemia (refer to Treatment of Hyperkalemia, NP16) adjust
dosages of medications cleared by kidney 3. definitive therapy
depends on etiology note: renal transplant is not a therapy for
AKI
Toronto Notes 2011
.Acute Kidney Injury/Chronic Kidney Disease (CKD)
Nephrology NP21
Prognosis high morbidity and mortality in patients with
sustained AKI and multi-organ failure
Chronic Kidney Disease (CKD)Definition abnormal markers (Cr,
urea) GFR 3 months or kidney pathology seen on biopsy or decreased
renal size on U/S (kidneys 50%) focal: some glomeruli affected
terms applying to an indMdual glomerulus global: entire glomerulus
abnormal segmental: only part of the glomerulus abnormal Types of
Changes proliferation: hyperplasia of one ofthe glomerular cell
types (mesangial. endothelial, parietal epithelial), with or
without inflammatory cell infiltration membranous changes:
capillary wall thickening due to immune deposits or alterations in
basement membrane crescent formation: parietal epithelial cell
proliferation and mononuclear cell infiltration from crescent-shape
in Bowman's space
bltdll: No sigricanl dillerence il uvivll hmrd NHD 11111 DlX.
Significlri survinl blllefitlor pllierQ _.dergoing LlX venus NHD.
Signliclnt rnonalty hmnllllia l'llll:tian willlllX
10.511MilllllllfliRe in hllll1l ratialor D1X Vlnlll NHD ralnlce.
Cancbin: lflllu mlllty1D DlX.lit is iriaricr1D llX.
wu
CIUII mlllbllty
Presentation of Glomerular DiseaseImportant Points To Remember
each glomerulopathy presents as one of 4 major glomerular syndromes
acute nephritic nephrotic rapidly progressive glomerulonephritis
asymptomatic urinary abnormalities each glomerulopathy can be
caused by a primary disease OR can occur secondary to a systemic
disease some glomerulopathy can present as more than one syndrome
at different times1. ACUTE NEPHRITIC SYNDROME
Clinical/Lab Features proteinuria (but 3.5 g/1.73m2/d)
hypoalbuminemia edema hyperlipidemia (elevated LDL
cholesterol),lipiduria (fatty casts and oval fat bodies on
microscopy) hypercoagulable state (due to antithrombin III, Protein
C and ProteinS urinary losses) patient may report frothy urine
glomerular pathology on renal biopsy: minimal change disease (or
minimal lesion disease or nil disease) - i.e. glomeruli appear
normal on light microscopy membranous glomerulopathy focal
segmental glomerulosclerosis (FSGS) membranoproliferative
glomerulonephritis nodular glomerulosclerosis each can be
idiopathic or secondary to a systemic disease or drug (sirolimus
can cause proteinuria without obvious glomerular pathology) Tabla
11. Naphrotic Syndroma Minimal
Prwentation -' Nepllratie Syndnlme 1. Sevn proteinuria (>3.5
Qfdl 2. Hypollbumilemia 3. Edama 4. Hyperlipidemia, lipiduria 5.
Oval fat bodies (microscopy( 6. Hypereoag!Jahle stile (antithrombin
Ill, protein Cand pnrtein S lost in urineI
Change
Membranous Glomeruloplllly HBV, SLE, solid breast. Gil
Focal S..-nlll Mambranoprolifaratiwe Glomeeulosderosis
Glomeeulonephrilil
Nodular Diabetes mellitus, amyloidosis
Secondary CIUSIS DI\IIICIIUIISTh. .py
Hodgkin's lymphomaNSAIDs
Reflux ne(h'opathy, HIV; HBV, obe&ity
HCV, malaria. SLE, leukemia, lymphoma, inlecl8d &hunt
Gold, penicillamine Heroin Recllce BP, ACB, &teroids
Steroids, ACEVARB fur proiBinuria Aspirin, ACEI, dipyridamole Treat
undBriying controversial cause
Steroids
The Nephritic-Nephrotic Spectrum glomerular pathology can
present with a clinical picture anywhere on a spectrum with pure
nephritic and pure nephrotic syndromes at the extremes (see Figure
15)Naphratic lntarmadiate
NaphriticHamatu.ria, "-
[ ProtainaraFSGS Membranous gtomarulopathyMinimal change
Membranoproliferative GN Focal proliferative GN lgA nephropllhy
ldioplllhic membranoprolifenrtive GN
Diffuse prolifen.tive GN Crescentic GN
HBV, HCV SL.E Cryoglobulinamia
Figura 15. Tha Spectrum of Glomerular Pathology
Toronto Notes 2011
Glomerular Disease
Nephrology NP25
3. RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS (RPGN)Clinical/Lab
Features a subset of nephritic syndrome in which renal failure
progresses in weeks to months crescent formation usually seen on
renal biopsy RBC casts and/or dysmorphic RBCs in urine classified
by immunofluorescence staining (see Table 12) treatment: underlying
cause for postinfectious; corticosteroids + cyclophosphamide or
other cytotoxic agent + plasmapheresis in select cases prognosis:
50% recovery with early treatment, depends on underlying causeTabla
12. RPGN Classification
RPGNTpl: AJrti.GBM m iltld .. %111RPGNC. 15% of cases
lmmuno.ftuorncence Linear pattern due to lgG 111d SUing Pattem C3
deposition along capillary loopsAntibodies against type IV collagen
in GBMPrimuyc....
RPGN Type II: Immune Complex miltlll24% of cases Granular
pattern due to subendlllhelial or subepithelial deposits DllgG and
C3 Most often di&sa&e
RPGN Type Ill: Non-immUDI lllldillld (i.e. piuci-immune)60'J(,
of cases
No immune stailingVasculitis of glomerular capillaries
Idiopathic Wegener's {c-ANCA +vel Microscopic polyangiitis (p-ANCA
+vel Cilurv-Stn!uss (ANCA -vel
z to systemic
Idiopathic anti.{lBM disease Goodpasture's disease
lgA nephropathy Post-infectious GN, SLE, Cryoglobulinemia,
Henoch-Sclxlnleil pLrpura
s-nduvc....
4. ASYMPTOMATIC URINARY ABNORMALITIESClinical/Lab Features
isolated proteinuria (usually 50 years old smoking other
atherosclerotic disease severe/refractory HTN and/or hypertensive
crises asymmetrical renal size increasing Cr with ACEUARB flash
pulmonary edema with normal LV function must establish presence of
renal vessel stenosis and prove it is responsible for renal
dysfunction duplex Doppler U/S (kidney size, blood flow): good
screening test (operator dependent) CT or MR angiography (effective
noninvasive tests to establish presence of stenosis) ACE inhibitor
renography (ie. captopril renal scan) renal arteriography (gold
standard)
ts
Investigations
Cancbin: llenllftly lt'I'IKIArizlti carries 5ignificlnt ri5b
Mhoullll'( beneil Ill nnl fln:tian oriiCOIIdlly11111:c1n1
cam!Bid1D
lllldUifliiiPI'
Treatment medical therapy, percutaneous angioplasty + stent,
surgical revascularization little or no benefit if therapy is late
Le. kidney is already shrunken. However, therapy can be considered
to save the opposite kidney if normal
3. RENAL VEIN THROMBOSIS
Etiology hypercoagulable states (e.g. nephrotic syndrome,
especially membranous), ECF volume depletion, extrinsic compression
of renal vein, significant trauma, malignancy (e.g. RCC), sickle
cell clinical presentation determined by rapidity of occlusion and
formation of collateral circulation acute: nausea/vomiting, flank
pain, hematuria, elevated plasma LDH, rise in Cr, sudden rise
in
proteinuria chronic: increasing proteinuria and/or tubule
dysfunction
Investigations renal venography (gold standard), CI' or MR
angiography, duplex Doppler U/S
Treatment anticoagulation with heparin then warfarin (1 yr or
indefinitely, depending on risk factors)
NP32 Nephrology
Vascular Diseasea of the Kidney/Systemic Diseases and the
Kidney
Toronto Notes 2011
Small Vessel Disease1. HYPERTENSIVE NEPHROSCLEROSIS see
Hypertension, NP32....... 1:11111 ..W*'ilm.Mid2lXXl; 17;133:600-3
cohort-wMII follow " of 5-I 0years. Pllilnll: 145 paliiJU w
iducilnxllnnlllllll crisis w11a inl6im111d li&2paaMh IICiari*w.
wllo did 11111 hm ranll crilil. need fordBy$is IIIII Ill\'
dalllllllllllg paliiJU Mil nlllli crilil . . . .: Six!y-0111
J*CII1I ol ptltilutlwitl-1 crilil good outx:ons (55 hid 110
diltflis 111d 3418C8ivld 11mPQIIIY dilllvsist onlv 4 rl 1bese
pllierQ chronic rellll fliUe 111d .-m-t dilllysil. Gllltlrlllln
50'1. ol .. patiarG wllo inibllv dilllysi5 3'II I Bmon1hs 1111r.
Farrt.nt dilytisw .t, dBIIII occ:uned in 31% ollhB plllilds.
c.Jailn: llllnllcrisis Cll1 M1111111Q11dwhn llypWnliol
contraiiiiiMIII ACE illlibibn
2. ATHEROEMBOLIC RENAL DISEASE progressive renal insufficiency
due to embolic obstruction of small and medium-sized renal vessels
by atheromatous emboli spontaneous or after renal artery
manipulation (surgery, angiography, percutaneous angioplasty)
anticoagulants and thrombolytics interfere with ulcerated plaque
healing and can worsen disease presentation: acute or chronic,
progressive renal dysfunction, labile hypertension, extrarenal
atheroembolic disease support diagnosis (livedo reticularis is a
classic sign) pathology: needle-shaped cholesterol clefts (due to
tissue-processing artifacts) with surrounding tissue reaction in
small/medium-sized vessels no effective treatment; avoid
angiographic and surgical procedures in patients with diffuse
atherosclerosis
3. THROMBOTIC MICROANGIOPATHY a spectrum which includes HUS,
TTP, DIC, post-partum renal failure renal involvement more common
in HUS than TTP renal involvement characterized by fibrin thrombi
in glomerular capillary loops arterioles treatment depends on cause
supportive therapy TTP: plasma exchange, corticosteroids
(splenectomy and rituximab if refractory) avoid platelet
transfusions and ASA
.... ..........
NEJM mrl; 251:2562-75 s.dJ; rftorrimd controlled iill will
IZIIIOIIIIfolcJw.q). l'llilnla: 1645 p!lients scheduled ta receilt
1
.........: NJrcoplalollfe COrticollaroidiiMd ailher.l) lillndl'd
dose cyct)IJIQ!ila; dlcianb iniLoction; 3) lowdou--.sv.idl dBcianb
iniLoction; 4) low doll illlhls Mil
4. SCLERODERMA 50% scleroderma patients have renal involvement
(mild proteinuria, high Cr, HTN) histology: media thickened, "onion
skin hypertrophy of small renal arteries, fibrinoid necrosis of
afferent arterioles and glomeruli 10-15% scleroderma patients have
a "scleroderma renal crisis": malignant liTN (usually within the
first few years), ARF, microangiopathy, volume overload, visual
changes, HTN encephalopathy renal involvement usually occurs early
in the course of illness treatment BP control with ACEI slows
progression of renal disease
Eslinalld Coc:tr.llft-Gd GfR 12 mollllulllrbnplllllllion.
....:1111 TICIGiilllllllm llllowllllignific:lndv hifi!BJ IGI'R It
12IIU!Ihl COIIfllld 111111 111111' M111 (65.4 mVmin VI. 51.1, 51.4,
56.7for IIIIlS I, 2. 4 reepeciMiy. lie TIICIIhlsn llso I'-d
dlclllllld IIIII riiCID 11jel:tion Ill 6 n.dls ll1d 12111111111svs.
II M111 (p30 minutes without spontaneous cessation or recurrent
seizures without full return to consciousness inter-ictally
ClassifieationSeiZU111UnpriiVOksd
...I
I
Provoked
...
+'. Panial- Simpla
can secondarily become - - - - - - - - - - - - - - - - -
Generahzad
t.I
...I
I
Complex
...
...Abet nee
Motor Sensory
Autonomic
+
Pwychiatric
...
l
Convulsive
...I
Fevar Metabolic Trauma
Clonic
Figura 1D. Classification of SaizurasStroke is the most common
cause of late-onset (>50 'f8lll' of age) seizures,accounting for
53-BO'K. of c__
Tonic
+ +
Tonio-Cionic
Myoclonic
+ ...
Atonic
Etiology idiopathic identifiable etiology: vascular, congenital,
neurodegenerative or other neurologic disorders, neoplasm, trauma,
childhood epilepsy syndromes, infection, metabolic, toxins, genetic
cryptogenic
Signs and Symptoms generalized seizures tonic-clonic (grand
mal): prodrome of unease or irritability hours to days before the
attack tonic ictal phase: tonic muscle contractions, arm flexion
and adduction, leg extension, 'cry' as respiratory muscle spasm and
air is expelled; lasts 10-30 seconds clonic ictal phase: clonus
involving violent jerking of face and limbs, tongue biting,
incontinence; 65 years of age have dementia common etiologies:
60-SO% Alzheimer's Disease (AD); 10-20% vascular dementia 85 years
of age accounts for 60-80% of all dementiasRisk Factors
family history of AD head injury
low education level smoking aluminum (controversial) Down's
syndromeSigns and Symptoms
cognitiveimpairment memory impairment for newly acquired
information (early) deficits in language, abstract reasoning, and
executive function psychiatric manifestations major depressive
disorder {5-896) psychosis (20%) motor manifestations {late)
parkinsonism (consider Lewy body disease)Investigations
perform investigations to rule out other causes of dementia as
necessary EEG: generalized slowing (nonspecific) MRI: dilatation
oflateral ventricles; widening of cortical sulci SPECT:
hypometabolism in temporal and parietal lobes
Treatment
acetylcholinesterase inhibitors have been shown to improve
cognitive function donepezil rivastigmine (Exelon), galantamine
(Reminyl) relative contraindications: bradycardia, arrhythmia, CHF,
CAD, asthma, COPD, ulcers, or increased risk of ulcers and GI
bleeding galantamine is contraindicated in patients with
hepatic/renal impairment memantine (Ebixa) is an NMDA-receptor
antagonist that has some benefits in later stage AD other -
although efficacy not proven ginkgo biloba Vit E (caution: >400
IU/day associated with excess mortality; Ievell evidence)
symptomatic management low dose neuroleptic trazodone for sleep
disturbance antidepressantsPrognosis
progressive mean duration of disease 10 years
Lewy Body Disease (LBD)Definition
progressive cognitive decline interfering with social or
occupational function; memory loss may or may not be an early
feature one {possible LBD) or two {probable LBD) of the following:
fluctuating cognition with pronounced variation in attention and
alertness recurrent visual hallucinations parkinsonism
Nl4 Neurolo8Y
Behavioural Neurolo8Y
Toronto Notes 2011
Etiology and Pathogenesis Lewy bodies (eosinophilic cytoplasmic
inclusions) found in both cortical and subcortical structures
Epidemiology 15-25% of all dementias Signs and Symptoms
:O.uctuation in cognition with progressive decline visual
hallucinations parkinsonism repeated falls sensitivity to
neuroleptic medications (develop rigidity, neuroleptic malignant
syndrome, extrapyramidal symptoms) REM sleep disorder Treatment
acetylcholinesterase inhibitors (e.g. donepezil) Prognosis typical
survival3-6 years
Frontotemporal Dementia (FTD)Definition progressive dementia
characterized by core symptoms of either disinhibition and
emotional lability or of apathy and detachment Etiology and
Pathogenesis gross pathology atrophy of frontal and temporal poles
microscopic pathology Pick bodies (intraneuronal inclusions
containing abnormal Tau proteins) Epidemiology 10% of all dementias
Signs and Symptoms core features behavioural disorder impairment of
personal conduct and of regulation of social interactions decline
in personal hygiene and grooming mental rigidity/inflexibility
perseverative and stereotyped behaviour speech and language altered
speech output (economy or pressure of speech)
echolalialperseveration physical signs primitive reflexes (ie.
pout, grasp, palmomental, glabellar) parkinsonism Investigations
MRI/SPECT - frontotemporal atrophy/hypometabolism
Creutzfeldt-Jakob Disease (CJD)Definition rare degenerative
fatal brain disorder Pathophysiology prion proteins causing
alterations in the brain such as spongiform changes, astrocytosis
and neuronal loss Epidemiology rare (1 in a million), peak
incidence between 50-70 years old
Toronto Nota 2011
Neurology NlS
Clinical Presentation sparadk CJD: rapidly progressive demenling
illness causing death within months, associatedwith myoclonus
cerebellar ataxia cxtrapyramidsl signs aldnelk mutism and
cortical bUndness sometimes occurfatalwlthinlyear EEG: triphasic
compleus
Diagnosis rule out treatable dementia, neurologic exam, EEG, MRI
only wsr.y to confirm diagnosis is brain biopsy/autopsy
1\fpes
sparadk CJD: most common form (8596), no risk facmrs hereditary
CJD: family history or tests positive fur genetic mutation (5-10%)
acquired CJD: transmitted via exporure to prion in nervous system
tissue (90% of essential tremor does not need treatment.
Differential Diagnoses 1. Tremor: a. Postural: physiologic,
anxiety, sedative/alcohol withdrawal, drug toxicity, heavy metal
poisoning, carbon monoxide poisoning, thyrotoxicosis, benign
essential tremor, cerebellar, Wilson's disease benign essential
tremor is a common autosomal dominant trait that presents as a
bilateral postural tremor of the vertical axis, especially in the
upper extremities b. Intention: brainstem lesion, cerebellar
lesion, alcohol, anticonvulsants, sedatives, Wilson's disease c.
Resting: Parkinsonism, Wilson's disease, mercury poisoningTable 17.
Approach to TremorsResting Body Part Characteristics Worse with
Associated Sx DDx Distal UE 3-7Hz pill rolling Rest while
concentrating "TRAP" IPD, Parkinsonism, Wilson's disease Sinemet,
anticholinergics, surgery, DBS Postural Uf/head/voice 612Hz fine
tremor Sustained posture (outstretched arms} Autosomal dominant
FHX
Intention Anywhere sensory) slowing, decreased
GBS is a neurological emergency due to risk of imminent
raspinrtory failtn.
....
,,
F-wave subtypes 1. Acute inflammatory demyelinating
polyneuropathy (AIDP) 2. Acute motor-sensory axonal neuropathy
(AMSAN) 3. Acute motor axonal neuropathy (AMAN) treatment disease
specific: IVIg or plasmapheresis nonpharmacologic: admit and
monitor vital signs and vital capacity due to risk of respiratory
failure, manage dysautonomia, manage pain prognosis nadir of
symptoms at 2-3 weeks, with resolution at 4-6 weeks 5% mortality
(higher ifiCU), 7-15% permanent substantial deficits Diagnostic
Approach to Peripheral Neuropathies 1. Differentiate: motor vs.
sensory vs. autonomic l. Pattern of Deficit: symmetry, focal vs.
diffuse, upper vs. lower limb, cranial nerve involment 3. Tempo:
acute to chronic, relapsing remitting vs. constant 4. Good History:
PMH, detailed family tree, exposures (e.g. insects, toxins, sex.
travel), systemic symptoms 5. Detailed Peripheral Neuro Bum: LMN
findings, differentiate between root and peripheral nerves, check
cranial nerves, check respiratory status
Miller-RICIH!r Y11rimt af GBS - Triild 1. Ophthalmoploqill
2. Ataxia 3. Arvllexil
....
,,
Mg and pi1Ui111apilemillalld tD morv rapid improvement, less
intensive care
and less ventillllion, but do not changemortality or ralaps1
ram.
N32 Neurolo8Y
Neuro-oncology/Neurom115Cular Junction Diseaaa
Toronto Notes 2011
Neuro-oncologyParaneoplastic SyndromesDefinition uncommon
complication of cancer; often is the presenting complaint
Pathophysiology likely an autoimmune attack on the nervous
sym:em by tumour antigens
Associated Neoplasms small cell lung cancer: cerebellar
degeneration, encephalitis, opsoclonus-myoclonus,retinopathy,
neuropathy, Lambert-Eaton syndrome breast: cerebellar degeneration,
encephalomyelitis, opsoclonus-myoclonus thymoma: myasthenia gravis
other syndromes: necrotizing myelopathy, motor neuron syndrome,
neuropathies, mononeuritis multiplex, polymyositis and
dermatomyositis, encephalitis
Investigations antibodies commonly ordered include anti-Hu,
anti-Ri and anti-Yo
Treatment unsatisfactory and often palliative. Options to
consider are steroids, IVIg, plasmapheresis and treatment of
malignancy
Tumours of the Nervous System see NS9
Neuromuscular Junction DiseasesClinical Approach to Disorders of
the Neuromuscular JunctionTabla 19. Common Disorders of the
Neuromuscular JunctionButuli1m
OculluAiulblr pamis
++ +N
++(early)
.....
', ..
Limb WIIDISS
htiguablity
Post-exen:ile enhlncement ReflexesANS anti:hulin. .ic Sx
+ + + +
+ ++
Dis1un of 1h1 niUilllllllscular junction typically feature
prominent fatiguability.
++GISSx
SansarySx
Associated conditionsRapatilivll EMG stimulatilll
Thymoma
Small cell carcinoma
"'
1' (rapid sti'I'IJiation)-.1- (slow
1' (rapid stimulation)>lr (slow stimulation)
Myasthenia Gravis (MG)Etiology and Pathophysiology damage and
blockade of post-synaptic acetylcholine receptors by specific
antibodies 15% of patients with myasthenia gravis have associated
thymic neoplasia, 85% have thymic
hyperplasia autoimmune disorder
Epidemiology bimodal age of onset - 20's (mostly women) and 60's
(mostly men)
Toronto Notes 2011 Signs and Symptoms
Neuromusc:ula.r Junction Diseasea
Neurology N33
see also Table 19 fatiguability and weakness of skeletal muscles
without reflex, sensory, or coordination abnormalities typically
ocular (diplopia/ptosis) -+bulbar (dysarthria/dysphagia) -+
necldlexors/extensors -+ proximal limbs respiratory muscle weakness
may lead to respiratory failure
Myasthenia Gravis is a neurological emergency due to 1he risk of
imminent rnpillllory failure I
....
,, ,,
Investigations edrophonium (Tensilon) test -can result in
respiratory difficulty so have crash cart nearby assess for
improvement over 2 minutes following edrophonium injection EMG
repetitive stimulation -+ decremental response single fibre
electromyography shows increased jitter (80-10096 sensitivity)
anti-acetylcholine receptor antibody assay (70-80% sensitivity)
MUSK antibody may be used if seronegative for AChR antibody CT/MRI
to screen for thymoma/thymic hyperplasiaTensilon is a drug 1hat
inhibit$ acltylcholinestlrllsl. It improvM mJscll function
immadilltaly in my811henia
gravis, but not in cholinergic crisis.
....
Treatment thymectomy 8596 of patients show improvement or
remission symptomatic relief acetylcholinesterase inhibitors (e.g.
pyridostigmine) does not affect primary pathologic process -+
rarely result in control of disease when used alone
immunosuppression steroids are mainstay oftreatment - 70-80%
remission rate azathioprine, cyclophosphamide and mycophenolate as
adjuncts to steroids or as steroid sparing therapy short-term
immunomodulation (for crises) IVIg and plasmapheresis
zClinical Forms rrf Mpltllenil GriVis 1. Ocular [15"'} 2.
Gene1111ized (85%1
Prognosis 3096 eventual spontaneous remission
Lambert-Eaton Myasthenic Syndrome (LEMS)Etiology and
Pathophysiology downregulation of presynaptic voltage-gated Calcium
channels 2 to specific channel binding antibody causing decreased
amounts of ACb released into the synaptic cleft 50-6696 are
ultimately associated with small cell carcinoma of the lung
Signs and Symptoms weakness of skeletal muscles without sensory
or coordination abnormalities reflexes are diminished or absent,
but increase after active muscle contraction bulbar and ocular
muscles affected in 25% prominent anticholinergic autonomic
symptoms (dry mouth >impotence> constipation > blurred
vision)
....
,,
Lambert-Eaton myas1hanic syndrome can be differentiated from
myasthenia Qlllvis, by 1ha phenomenon of postexercise
facilitlltion.
Investigations edrophonium test (see Myasthenia Gravis) -+ no
response EMG: rapid (> 10Hz) repetitive stimulation -+
incremental response screen for malignancy, especially small cell
lung cancer post-exercise facilitation- an incremental response to
repetitive stimulation due to presynaptic calcium accumulation
Treatment tumour removal acetylcholine modulation increased
acetylcholine release (3-4 diaminopyridine) decreased acetylcholine
degradation (pyridostigmine) immunomodulation steroids,
plasmapheresis, IVIg
N34 Neurolo8Y
Myopathiea
Toronto Notes 2011
MyopathiesClinical Approach to Muscle DiseasesTable 20.
MyopathiesEtiology lnlllmmiiDry Polymyositis Mya[gies Pharyngeal
involvement Mya[gias Similar to polymyositi& Characteri&tic
r.&les Can be paraneoplastic
Ksr lnvatigations1' CK Biopsy: endomesial Necrosis 1' CK Biopsy:
parifasciculll' atrophy
....
',rnsen.tion
Dermatomyositis
lmporu,nt lnfanution to Reganllnf Myapllthilll Weakness:
proximal > distal
Pain: myalgias, but no impaired MyotDnil [difficulty with
relaxldioo)
Sarcoido8is Inclusion body myositis
ACE IIMII Biopsy: IJliiUIOIIllls
Weak quads and deep finger flexorsSee Endocrinology
1' CK Biopsy: ilclusion bodias TSH, serum cortisol, calcium
panel Toxicology Biopsy: selective loss of thick Myosin
filaments
.....
',
Endoc:rin1
Thyroid (1' or -1-) Cushing's syndrome Parathyroid (1' or -1-)
Medication Critical illness myopathy
Myoplllllisl1118 chlllle1llrizad by prominent symmetric
proximal
Medication or toxin history
weakness end lbsant SIIIIIO!'f chlngal.
.....
',Hereditary Dystrophy
ICU patient Hx steroid& and nondepolarizing palltfzing
agents Faiure to ween from ventilationMya[gies Inflammatory
myopathy onset {Duchenne and Becker) Prograssiw proxi11111l muscle
-knass pseudohypertrophy Distal myopathy Myotonia Genetic
anticipation Exercise-related rnyalgias, cramping, and
myoglobumimria Episodic W8ilkness between attacks
Parasitic, bactErial, or vinll Duchenne
1' ITI'fl9obin Biopsy: abnormal dyttrophin Staining Genetic
testing
Good Cll..ti- to Alina Proximal
wen-s
Legs: climbing slllirl, stand from sit Anna: n111ch above
hlllld, wash hair
BecksrMyotonic dystrophy
.....
',
Hereditary Mltlbolic
McArdle's
Common Mellicalio1111bat Cauu Mpptllhy Steroids, mrtins and
IIIT!mnmrBis
1' lactate 1' serurnturinary myoglobil Pllst-sxen:ise 1'cr-I-K
Increased lactate Biopsy: ragged red fibres
Heredililry Periodic Parllylil Heredililry
Periodic paralysis MERRF MELAS ICI!ImsSayre
Mitochandriil
Ptosis, conmon Proximal > distal myopathy Exercise
intolerance Rhabdomyolysis
Abbreviltion5: MBliiF -ITilochoncnl encephlllomyoplllhy
slrulie-like episodes
rauged llld fibe11; MELAS- mitochondrial encepllllomyopathy,
lactic I!Cifbis, and
Polymyositis/Dermatomyositis see RH13
Myotonic DystrophyEtiology and Pathophysiology unstable
trinucleotide repeat in DMK gene (protein kinase} at 19ql3.3 number
of repeats correlates with severity of symptoms; autosomal dominant
Epidemiology most common adult muscular dystrophy prevalence
3-5/100 000 Signs and Symptoms appearance: ptosis, bifacial
weakness, frontal baldness {including women), triangular face
giving a drooping/dull appearance
Toronto Notes 2011
Myopathies/Cerebellar Disorders
Neurology N35
physical exam distribution ofweakness: distal greater than
proximal (in contrast to other myopathic disorders) myotonia:
delayed relaxation of musclc:s after exertion (elicit by tapping on
thenar muscles with hammer) cardiac: 90% have conduction defects (
1 heart block; atrial arrhythmias) respiratory: hypoventilation 2
to muscle: weakness ocular: subcapsular cataracts, retinal
degeneration, decreased intraocular pressure EMG: subclinical
myotonia -long runs with declining frequency and amplitude
Treatment no cure management of myotonia: phenytoin
Duchenne and Becker Muscular Dystrophy see Pediatrics, P46
Cerebellar DisordersClinico-Anatomic Correlations vermis:
trunk/gait ataxia cerebellar lobe (i.e. lateral): tremor, rebound
phenomenon, dysarthria, dysdiadochokinesis, nystagamus Symptoms and
Signs of Cerebellar Dysfunction nystagmus: observe on extra-ocular
movement testing (most common is gaze-evoked nystagmus) dysarthria
(ataxic dysarthria): abnormal modulation of speech velocity and
volume- elicit scanning/telegraphic/slurred speech on spontaneous
speech (see Dysarthria, Nl9) ataxia: broad-based, uncoordinated,
lurching gait dysmmetria: irregular placement ofvoluntary limb or
ocular movement dysdiadochokinesis: unable to perform rapid
alternating movements (e.g. pronationsupination task) postural
instability: look for truncal ataxia on sitting (titubation
=rhythmic rocking of trunk and head); look for difficult tandem
gait and broad based gait intention tremor: elicit on
finger-to-nose testing- typically orthogonal to intended movement,
and increases as target is approached hypotonia: decreased
resistance to passive muscular extension- occurs immediately after
injury to lateral cerebellum pendular patellar reflex: knee reflex
causes pendular motion ofleg occurs after injury to cerebellar
hemispheres rebound phenomenon: overcorrection after displacement
of a limb (with both arms extended --+ pushing both will cause one
to rebound up if there is lesion on that side)
Wernicke-Korsakoff Syndrome deficiency of thiamine due to
alcohol abuse acute: apathy, confusion, decreased EOM, ataxia
(truncal and gait) without treatment progresses to encephalopathy
and ultimately death treatment: thiamine 100 mg Korsakoff's
syndrome: progressive decline ofboth anterograde and retrograde
memory note that alcohol can also cause a cerebellar ataxia
separate from thiamine deficiency. The ataxia can be due to
cerebellar atrophy or alcohol polyneuropathy
Cerebellar AtaxiasCongenital Ataxias early onset nonprogressive
ataxias associated with various syndromes as well as development
abnormalities (e.g. Arnold-Chiari malformation, Dandy-Walker cysts)
Hereditary Ataxias autosomal recesaive: includes Friedreich's
ataxia, ataxia telangiectasia, vitamin E deficiency Friedreich's
ataxia: prevalence 2/100 000; onset between 8 and 15 years signs:
gait and limb ataxia, weakness, areflexia, extensor plantar reflex,
impaired proprioception and vibration death in 10-20 years from
cardiomyopathy or kyphoscoliotic pulmonary restriction autosomal
dominant: spinocerebellar ataxias (SCA.s) of which 30 exist, most
are CAG repeats
N36 Neurolo8Y
Cerebellar Disorden/Vertigo/Gait Diaturbances/Pain Syndromes
Toronto Notes 2011
Acquired Ataxias neurodegeneration (e.g. multiple system
atrophy) systemic: alcohol, celiac sprue, hypothyroidism, Wilson's,
thiamine deficiency toxins: carbon monoxide, heavy metals, lithium,
phenytonin, solvents vascular: infarct, bleed, basilar migraine
autoimmune: MS, Miller-Fischer (GBS) children: tumours,
post-viral
Vertigo see Otolaryngology, OT12
Gait DisturbancesApproach to Gait Disturbances I. Length of
stride if small paces - look at posture if stooped with no
armswing- Parkinsonian gait look for other signs of extrapyramidal
disorders if upright with exaggerated armswing - Marche a petit pas
due to diffuse infarction of both cerebral hemispheres
(lacunar)
r-t,
CENTRAL MOTOR SYSTEMS 3 compnnb tu til cantrol af pit 1.
Pyramidal: main ouUiow from cor1ex to spinal cord 2.
Extrapyramidal: bani ganglia inhibita BJa:llll mCMimanb; 3.
Clrlblllum: afflcts coordination of
2. If normal stride length, look at width between feet if
wide-based- ataxia if high stepping and positive Romberg- sensory
ataxia loss of joint position sense (+ve Romberg) if wide based
without high stepping - cerebellar ataxia veers to side of the
lesion if scissoring of legs or toe walking- spastic gait bilateral
circumduction due to spastic paraparesis from cerebral palsy,
multiple sclerosis or cord compression 3. If normal width, look for
height of step if high stepping bilaterally- bilateral foot drop if
feet barely leave ground or disjointed movement - magnetic/apraxic
gait frontal lobe pathology due to normal pressure hydrocephalus or
cerebrovascular disease4. If no high stepping, lookfor stabllity of
pelvis if rotation of pelvis - waddling gait
proximal muscle weakness due to congenital deformity or
myopathy5. If no waddling, look at symmetry if asymmetric -
antalgic gait, deformity or hemiparetic gait antalgic gait is due
to pain from an MSK problem hemiparetic gait involves a foot drop
and circumduction of spastic leg due to UMN lesion
6. If movement is elaborate and inconsistent, especially when
being observed. conaicler functional pit rule out an odd gait due
to chorea from Huntington's disease
Pain SyndromesApproach to Pain Syndromes
...._,, Pinprick CIIUUI sharpnns rnldimd byJIIJfibani Pain to
damage is mediated by Cfibres
Definitions Nociceptive pain: pain arising from normal
activation of peripheral nociceptors Neuropathic pain: pain arising
from direct injury to neural tissue. bypassing nociceptive pathways
Spontaneous pain: unprovoked burning, shooting, or lancinating pain
Paresthesiae: spontaneous or evoked abnormal nonpainful sensations
(e.g. tingling) Dysesthesiae: spontaneous or evoked pain with
inappropriate quality or excessive quantity Allodynia: a
dysesthetic response to a nonnoxious stimulus Hyperalgesia: an
exaggerated pain response to a noxious stimulus
Toronto Notes 2011
Pain Syndromes
Neurology N37
Medical Pain Control primary analgesics: OTCs, opiates
adjuvants: antidepressants (TCAs, SSRis), anticonvulsants
(gabapentin, carbamazepine), baclofen, sympatholytics
(phenoxybenzamine), a2-adrenergic agonists (clonidine,
pregabalin)
Surgical Pain Control direct delivery: implantable morphine pump
central ablation: stereotactic thalamotomy, spinal tractotomy or
dorsal root entry lesion peripheral ablation: nerve blocks, facet
joint denervation deep brain stimulation (DBS) or dorsal column
stimulation
Neuropathic PainDefinition pain resulting from a disturbance of
the central or peripheral nervous system
Symptoms and Signs hyperalgesia/allodynia subjectively described
as -burning, heat/cold, pricking, electric shock, perception of
swelling, numbness (Le. stocking/sock distribution) can be
spontaneous or stimulus evoked distribution may not fall along
classical neuro-anatomicallines
Associated Issues sleep difficulty anxiety/stress/mood
alteration sexual dysfunction
Causes of Neuropathic: Pain peripheral neuropathy systemic
disease - diabetes, thyroid disease, renal disease, rheumatoid
arthritis nutritional/toxicity- alcoholism, pernicious anemia,
chemotherapy infectious - HN trauma - post surgical, nerve injury
nerve root: post-herpetic neuralgia, cervical and lumbar
radiculopathies, tic douloureux (see Trigeminal Nerve, Nl8),
plexopathies central: MS, post-stroke, phantom limb, spinal cord
injury Complex Regional Pain Syndromes (see N38) malignancy
Treatment pharmacotherapy: TCA. SNRI, anticonvulsant, long
acting opiate, topical lidocaine, capsaicincream, intrathecal
opioid or clonidine, Botox, nerve block surgical therapies: dorsal
column neurostimulator, DBS (thalamus) other therapies:
neuropsychiatry - cognitive behavioural theraphy, psychotherapy
rehabilitation - physiotherapy CAM - acupuncture, meditation,
massage therapy, TCM
Tic Douloureux (Trigeminal Neuralgia) see Trigeminal Nerve,
N18
Postherpetic Neuralgia (PHN)Definition pain persisting beyond 3
months in the region of a cutaneous outbreak ofherpes zoster
Etiology and Pathogenesis destruction of the sensory ganglion
neurons (e.g. dorsal root, trigeminal, or geniculate ganglia)
secondary to reactivation of herpes zoster infection
Epidemiology 10-15% of all patients with cutaneous herpes zoster
>80% of herpes zoster infected patients >80 years old
N38 Neurolo8Y
Pain Syndromes
Toronto Notes 2011
Signs and Symptoms types of pain: constant deep ache or burning.
intermittent spontaneous lancinating/jabbing pain, allodynia
distribution: thoracic > trigeminal > cervical > lumbar
> sacral Treatment acute herpes zoster early treatment with
antiviral agents (acyclovir; longer-acting famciclovir and
valaciclovir more effective) may prevent PHN in patients over 50
years PHN medical: TCA, pregabalin, gabapentin, opiate, lidocaine
patch, intrathecal methylprednisolone surgical: spinal tractotomy,
dorsal root entry zone lesion
Complex Regional Pain Syndromes (CRPS)Definitions CRPS is a pain
syndrome characterized by the following 1. presence of an
initiating noxious event 2. continuing pain, allodyrua, or
hyperalgesia with pain disproportionate to inciting event 3.
evidence during the course of symptoms of edema, changes in skin
blood flow, or abnormal vasomotor activity 4. absence of conditions
that would otherwise account for degree of pain and dysfunction
Classification CRPS type I (reflex sympathetic dystrophy): minor
injuries of limb or lesions in remote body areas precede onset of
symptoms CRPS type II (causalgia): injury of peripheral nerves
precedes the onset of symptoms Signs and Symptoms stage I (acute)
pain: burning or aching disproportionate to initial injury
autonomic: edema and temperature inequality stage II (dystrophic)
pain: constant and increased by stimulus to affected part
autonomic: osteoporosis, cool hyperhydrotic skin, hair loss,
cracked/brittle nails stage III (atrophic) pain: paroxysmal spread
autonomic: thin, shiny skin, thickened fascia with contractures,
bony demineralization Investigations diagnosis is clinical trial of
differential neural blockade may be helpful Treatment medical:
phenoxybenzamine (sympatholytic) surgical: paravertebral
sympathetic ganglion blockade
Thalamic Pain (Dejerina Roussy Syndrome) - -Definition
hypersensitivity to pain as a result of damage to the thalamus
Etiology and Pathogenesis injury to ventral posterolateral (VPL)
and ventral posteromedial (VPM) nuclei of the thalamus ischemic
stroke hypertensive vascular hemorrhage Signs and Symptoms begins
with hemianesthesia then persistent spontaneous burning
contralateral to lesion altered response to light cutaneous and
deep painful stimuli Treatment medical: amitriptyline,
anti-convulsants surgical: stereotactic thalamic stimulation (may
increase sensory deficit)
Toronto Notes 2011
Headache
Neurology N39a.lllliaal cmc.J Eumilllllign: O.llil Pllilnt wilb
11Hdde .... a..,. NllllJWA 2006; 2!1&:1 274-83
HeadacheClinical Approach to HeadachesInvestigations good
history and physical to rule out serious causes of headache
important aspects of neurologic exam: LOC and MSE, pupils
(symmetry), fundi (papilledema, retinal hemorrhages), pronator
drift, meningismus, deep tendon reflexes and Babinski, gait
indications for a new-onset headache, worst headache of life,
thunderclap headache, headache with worrisome symptoms (fever,
meningismus, altered LOC, focal neurologic deficits, trauma,
papilledema, morning headache) if CT is negative but suspicion of
SAH or meningitis, perform a lumbar puncture
N......,nnmanic: p-
Dnltlil!lllillllwilb ........... The most of..- for dilgnosing
nipile i$ .urrrrm.d by 11-. P(Utling
'*"
u-
a - 4inl1ion of 4-72
UnilideriiiOCIIion
cr
N - Nlu or-womiling D- Disllblingint!llsily
Table 21. Headaches- PrimaryTCIIIioa-Typa PrevalenceMigrma
..............,
ThaiR far dafiW or polllil1i n-i11111inl dill!jlllllii
VlrillwM!I U.lllmblr rlfiiUM pr8I8IE Mdl 3111d feiW U.Llls ... 24
{1.5-3181. 3.5 {1.3-9.2111111 0.41 {0.32-0.521 TllpiC1ivltf.
Dnlllil , . . .... h...... IIIII
Clustar M Nona Bilateral frontal MinLIII!s-days lndual; worse in
PM Band-like; constant Mild-modarata DepressionAnxiety
12% 10-30 F>M
Aga of OlllltSexBia Family HistaiY
M>F
+++Uniateral>bilateral Fronto-tenwal Haurs-days Gradual;
worse in PM Tlrobbing Modarata-severa Noise Light Strainilg Coujing
Activity Rest Nausi!I1/VDmiting Photo/phonophobia Aura Muscle
tension in scall)'neck Tandar scalp artaias AcuteRx MA NSAIDS
Triptans Ergotamine Prophylaxis l'ropnllolol TCA
Anticonvulsents
+Retroorbilll 10mh-2. haurs
l.ocatiCIIDul'llion Onset/CGune
The prawlence rl ii'Uicllnill pllllology {!111111
problliiitylwrias lnlll011 v.1lh dlronic helldldle 1he plellllence
is l.l'J. {0.77-1.11\).ln Ylll niglint-typl lllldlclw the prMiince
is Howavll. inlhose prasal1ing wi1h new lllldlclw the prMiince is
32'Jo in 1hose jiiUidiiQ Ylilll t!UIIIarcllp hlllldlchl the prMimct
is 43\ {211-611\). Ill th8le dilllrant popullbs. 110 clinical
flllfln was found lo hlllllful inlllivJ imcrlrill pethoQ in a
1118111iniiUMYHawM!. -a indivi!UI c1inicll IIU.ns Will luund 1o 1xt
]IIICictive of lignili:lnt petholoQr.c:QI8r-tp haadache
Daily headache for weeks, months, nocturnalConstant, aching.
stabbing S8\111'8 (waklls from sleep) Light
abnonnlllraJroiDQicll1111111111ddneli-typl hlldlch1
DualitySeverity Pravoldng
10.7 {21-52) 5.3 {2.4-12) 3.8 {2.0-7.11
IQUIMbld
lllldlclwv.tiilllldlclw Mil wmiling
3.2 {1.66.61 2.3 {1.4-UI1.8 {112.61
EtOH
Noise Hunger Slaap deprivation Pallating Rest No vomiting No
photophobia Muscle tension i'1 Non1)harmacological Psychological
counseling Physical modalities (e.g. heat, massage) Phannacological
Simple analgesics Tricyclic antidepressants
Walking around
ARoc:iltad Sx
Red watery eve Nasal congestion or rhinoi'Thea Unilateral
Homer's Red watery eye, rhinorrhea Eyaid !hopAcute Rx Oz
Sumatriptan (IIIISII or injection) Prophylaxis Verapamil Lithium
Methylsergide Pnmisolone
Six Dl Seria Halldac.._ lnaluda: 1. The lUdden onset Ill a
savm
headache;
Pllysicll SignsMIRII!IIdllnt
neurolovic deficibi; or 3. New headaches beginning after age
50.
2. AccomplfTYing impaired mental sbllus, uizul"ls, or focal
fl-.
Table ZZ. Headaches- SeriousMeningllllrrilatilll Incidence Age
of Onset SP:Bils Locetion Duration Onset/Coull8Quilty
...creased lllraa'anill Pressure
