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7/21/2019 Updated Mini Exam 6 Review
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MINI-EXAM
#6 REVIEW
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The cingulate, septal,orbitofrontal, sensory andmedial prefrontal corticalregions have major inputsto the hypothalamus.
The insula connects withthe hypothalamus andbrainstem ANS centers.
You have no consciouscontrol over ANS responseto emotions.
Review
orte! via "imbicSystem to
#ypothalamus
to ANS
ANS $ %motions
enters in thebrainstem reticularformation and theNTShelp coordinatethe activities of theANS. These brainstem
areas receive a&erentsfrom the h othalamus
NT
S!
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The 'orsal "ongitudinal (asciculus )'"(* is the major pathwayconnecting the hypothalamus with the ANS. The hypothalamuscontrols the ANS+ it is the "head anlion$.
rainstem lesions can disrupt spinal ANS.
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-T#% A'R%NA"NR/S#.0
The adrenal medulla,acting via the releaseof adrenaline into theblood stream, spreadthe e&ects of
generali1edsympathetic activity toall cells of the body.lood shunted from 2
system and s3in to NSand s3eletal mm.
Release of glucose+increased heart rate $
contractility+ increased
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R%2/"AT4N 4("44' 5R%SS/R%
lood pressure isconstantly monitoredthrough input from thebaroreceptors in the
carotid sinus and aorticarch
Orthostatic hypotension,
an acute decrease inblood pressure whensuddenly assuming anupright positionindicates an interruptionof the baroreceptor
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SNS %ia &el%ic &le'us()res*n( neurons in +,.!
)SNS
SNS is tonicallyinhibiting the5SNSfrominitiatingdetrusor
contraction $tonicallyconstricts theinternalurethral
sphincter.
S789
MI/T0RITI1N/ENTERS/orte': Sup. frontalgyrus
2rainstem: 5ons)arrington;s nucl.*
'escending control
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The level of NS injurydetermines bladder function.
Note: an uninhibitedbladderis a result of injuryto the NS above the ponsthat disrupts higher NSpathways to the pons. -An
infantile bladder.0
5athway from pontinestorage area disrupted.ladder walls contract
upon minimal stretch.No control over e!ternal.urethral sphincter.
No a&erent or e&erentinformation to or frombladder.
2+A77ER 0N/TI1N8 +ESI1NS
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'amage to the 5SNS will result in problems with voiding the bladder. fthe damage is abo%e s&inal sements S.-9a RE+EX)old term >spastic* neurogenic bladder will result. There are two types of re6e!ive
bladder: uninhibited and automatic.
?ith the uninhibited re:e' bladder, the lesion lies above thelevel of the pons. Since the pontine storage and micturition centers areintact )but voluntary control over these centers are lost* the bladder
completely empties whenever it gets full 8 just li3e in an infant. ?ith an automatic re:e'i%e bladder, the damage is below thepontine storage and micturition centers, but above S789. n thiscondition, the bladder wall contracts with just minor pressure)generated by the presence of urine* within the bladder. Since thevoluntary control over the e!ternal urethral sphincter is lost, the
bladder has fre@uent involuntary voiding which never completelyempties the bladder.
f the spinal cord is damaed at S.-9, or if the cauda e@uina islesioned, a N1N-RE+EX)old term > 6accid* neurogenic bladder will
result. n this case, there are no visceral sensory
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'isruption of SNS to thehead can occur in spinalcord lesions above TB,
ventral root lesions ofspinal nn. TB8C, traumaanywhere along cervical $upper thoracicsympathetic chain, traumato internal carotid n. or the
internal carotid a. )afterthe n. joins it*, as well asdisruption of descendinginputs from thehypothalamus to thebrainstem or cervical
spinal cord.
HORNER SYNDROME
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Hirschprungs disease
Also called congenital aganglionic megacolon %!treme dilation and hypertrophy of the colon,
with fecal retention Absence of anlion cells in the m*enteric
&le'us )neural crest cells fail to migrate into thecolon*
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Familial dysautonomia (Riley-Day syndrome)
Autosomal recessive disorder characteri1ed byabnormal sweating, unstable blood pressure,
diDculty in feeding )inade@uate muscle tone inthe 2T*, and progressive sensory loss
+oss of neurons in autonomic and sensor*anlia
5redominantly a&ects Eewish childrenTo determine whether or not a patient has an
intact sympathetic innervation, a small s3insample is surgically removed and prepared for
immunostaining with antibodies againstNE0R1)E)TI7E ; released by manysympathetic postganglionic fbers, includingthose that innervate blood vessels of the s3in
2enerally, sympathetic ganglion cells usenore ine hrine rather than e ine hrine as a
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Raynaud syndrome
Painul disorder of the terminal arteries of thee!tremities
haracteri1ed by idiopathic bilateral cyanosis ofthe digits, due to arterial and arteriolarconstriction caused by emotion or cold
Treatment8 )reanlionic s*m&athectom*
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Shy-Drager syndrome nvolves preganglionic sympathetic neuron Now considered as an entity of M0+TI)+E S;STEM
ATR1)
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5rimary brain tumors.
Feninges: meningioma 2lia 8
Astrocytes 8 astrocytoma 4ligodendrocytes 8 oligodendroglioma
%pendyma G ependymoma, choroid ple!uspapilloma, colloid cyst )Hentricles*.
5rimitive cells: -blastoma0 e.g.neuroblastoma.
Neuronal I: ganglioglioma, gangliocytoma Nerve sheath: schwannoma, neuro
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linical features:
Raised ntracranial 5ressure.#eadache, vomiting, slow pulse,
papilledema. "ocaldamage:Nerve $ tract de
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Feningiomas
5redominantly benign tumors ofadults, usually attached to the dura
Arise from the meningothelial cell of
the arachnoid
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Feningioma:
ommon sites: parasagittal )fal!*, sphenoidridge, olfactory groove (emales common )7:B*
?ell demarcatedG ompression 8 Nonvasion
Ficroscopic: whorls and psammoma bodies #yperostosis over the tumor.
Slow growth, well di&erentiated, no spread)enign*.
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#istologic patterns
Syncytial8 whorled clusters of cellsthat sit in tight groups without visiblecell membranes+
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At medium power, this meningioma is composed ofwhorled nests of cells. A variety of patterns are
possible.
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5sammoma bodies
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Astrocytoma
AstrocytomaG ommonest tumorsof adults. )JKL*
?ell di&erentiated, slow growing. enign 8 but malignant behavior.
n
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Astrocytomas
Adults: Supratentorial )erebrum*,
Solid, Falignant, (ibrillary
hildren: nfratentorial )erebellum*,
ystic, enign, 5ilocytic
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(ibrillary astrocytomas
2rossly solid ommon in cerebral hemispheres
"ow grade in young, higher grade
in older 2rading
'i&use astrocytoma )low grade*
Anaplastic astocytoma2lioblastoma multiforme )high
grade*
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2lioma:
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2lioblastoma Fultiforme G foci of necrosis withpseudopalisading of malignant nuclei
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(ibrillary astrocytoma: microscopic
"ow grade8 hypercellularity,pleomorphism
Anaplastic8 as above plus mitosis,vascular endothelial proliferation
2lioblastoma multiforme8as aboveplus necrosis and pseudopalisades.2rossly variegated appearance)multiforme*
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2lioblastoma
Necrosis in serpentine pattern8occurs in areas of hypercellularity with
highly malignant tumor cells crowdedalong the edges of the necroticregions,
5roducing a histologic pattern Gpseudopalisading
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2lioblastoma
Hascular cell proliferationis characteri1edby tufts of piled8up vascular cells thatbulge into the vascular lumen+
The minimal criterion is a double layer ofendothelial cells.
?hen vascular cell proliferation ise!treme, the tuft forms a ball8li3estructure, the glomeruloid body
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5ilocytic astrocytoma
ommon in childhood Fost slow growing of the gliomas
Fost childhood brain tumors arise below
the tentorium, which is the reverse of theadult.
Sites: cerebellum, around H., optic nerve
2rossly cystic with mural nodule Ficroscopic elongated hair8li3e )pilo* elongated cells Rosenthal
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5ilocytic astrocytoma8 bipolar cells with long, thinMhairli3eM processes that are 2(A58positive+ Rosenthal
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4ligodendroglioma
The lesions are found mostly in the cerebralhemispheres, with a predilection for white matter.
(rontal lobe mass with areas of calci
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Tumors are composed of sheets of regular cells with sphericalnuclei containing
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%pendymoma
Arise ne!t to the ependyma8lined ventricularsystem
occur near the fourth ventricle
%nlargement of the lateral ventricles with ahomogenous, well8circumscribed mass within thefourth ventricle.
The mass e&ect can produce an obstructivehydrocephalus.
The headaches are associated with dull pain andseem di&use, in time will become more fre@uent
and prolonged.
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The microscopic appearance of an ependymoma reveals a rosettepattern with the cells arranged about a central vascular space. t is
histologically benign. )5erivascular pseudorosettes*
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Fedulloblastoma #ighly malignant cerebellar tumor.
)primitive neuroectodermal tumor*
an compress 9th ventricle, causinghydrocephalus
'issemination through the S( is acommon complication,
5resenting as nodular masses elsewhere inthe NS,
metastases to the cauda e@uina that aresometimes termed MdropM metastasesbecause of their direct route ofdissemination through the S(.
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Neuro
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Fultiple neuro
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Schwannoma
?ell8circumscribed
%ncapsulated massesthat are attached to the
nerve but can beseparated from it
(irm, gray masses
'iscrete
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The mass lesion here is arising in the acoustic)eighth cranial* nerve at the cerebellopontine angle.
This is a schwannoma. 5atients may present with
hearing loss.
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5eripheral nerve tumors
Schwannoma Schwann cells
Compress the nerve trunk
Encapsulated
Easily resectable without nerve
damage Microscopic:
Antony A and B fibers
Verocay bodies
eurofibroma Schwann cells! neurites!
fibroblasts
"usiform and involves nerve trunk
ot encapsulated
ot resectable without sacrificingnerve
Micro# $ntermingled cells withwavy nuclei
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Neuro
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Neuro
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N(
The NF1gene, located at [email protected],has been identi
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Tuberous Sclerosis
1. Dominant inheritance
2. Clinical triad:seizuresmental retardation
adenoma sebaceum
3. Retinal hamartoma (phakoma)
. !ubers (hamartomas) in cerebral corte"
#. $ubepend%mal &iant cell astroc%toma
'. amartomas in other or&ans: heart kidne%
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S3in lesions are common in tuberous sclerosis
MAsh leavesM8 white lesions lac3ing normal s3incolor that have the shape or appearance of an ashleaf and may appear anywhere on the body.
Shagreen patches: These appear on the lower bac3as raised patches of s3in with an orange8peelte!ture.
Adenoma sebaceum )angio
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Tuberous Sclerosis
The more commonly mutatedtuberous sclerosis locus )TSC2* is
found on chromosome BQpBC.Candencodes a protein )tuberin*
Hon #ippel "indau
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Hon #ippel8"indau'isease
An autosomal8dominant disease inwhich a&ected individuals developtumors )capillary hemangioblastomas*
within the cerebellar hemispheres, theretina, and, less commonly, thebrainstem and spinal cord.
ysts involving the pancreas, liver, and3idneys and have a propensity to
develop renal cell carcinomaof the
2 f #i l "i d
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2ene for von #ippel8"indaudisease
A tumor8suppressor gene, is locatedon chromosome Cp787Q and
encodes a protein )pH#"*4ne of the targets of the comple!containing pH#" is hypo!ia8induced
factor B )#(8B*,a transcription factorinvolved in regulation of e!pressionof H%2(
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Sturge!eber syndrome)also called encephalotrigeminal angiomatosis*
A rare congenital disorder associated with venousangiomatous masses in the cortical leptomeninges andipsilateral facial port wine nevi+
Fental retardation, sei1ures, hemiplegia, and s3ull radioopacities also occur.
Thus, a large acial "ascular malormation in a child withmental defciency may indicate the presence o moree#tensi"e "ascular malormations
2laucoma: sites of action
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2laucoma: sites of action
Site of action of miotics in anleclosure glaucoma: contraction of
sphincter pupillae removes pupillarybloc3 and removes the obliteration ofiridocorneal angleSite of action of miotics in o&en anleglaucoma: contraction of ciliary musclepulls on scleral spur and improves
trabecular patencySite of action of )a* bloc3ers )b* Bagonists )c* 7 agonists )d* carbonicanhydrase inhibitors: all reduce a@ueoussecretion by acting on ciliary bodySite of action of prostaglandins and
possibly adrenaline: increaseuveoscleral out6ow by alteringpermeability andor pressure gradientsSite of action of adrenaline: possiblyincreases a@ueous conductivity oftrabecular filtering cells )7 action*
B
B
7
C
9
0%eoscleral out:o=
Trabecularout:o=
S&hincter&u&illae
2laucoma
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>+A0/1MA8f the normal a@ueous humor 6ow
through the scleral venous sinuses isbloc3ed, pressure builds up in theanterior and posterior chambers of theeye compressing the retina and theretinal arteries resulting in blindness, acondition called GLAUCOMA
1&en?=ide anle laucoma: 5rimarycause is un3nown. Seen in elderly.Secondary causes include uveitis, trauma,corticosteroids and vasoproliferativeretinopathly that can obstruct or decrease
the 6ow of a@ueous humor. 5eripheralvision lost
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7rus for o&en?=ide anle laucoma:5rostaglandin analogues:
'rugs: "atanoprost, bimatoprost, travoprost Fost fre@uently used antiglaucoma medicines ncreasing uveoscleral out6ow, possibly by
increasing permeability of tissues in ciliary muscle or
by an action on episcleral vessels lurring of vision, increased iris pigmentation)browning*, thic3ening and dar3ening of eyelashes
arbonic anydrase inhibitors:
'rugs: aceta1olamide "imits generation of bicarbonate ion in the ciliary
epithelium No pupillary or vision changes
2laucoma drugs
2laucoma drugs
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7rus for o&en?=ide anle laucoma:holinomimietics:
'rugs: 'irect )5ilocarpine, carbachol*+ ndirect)5hysostigmine, echothiphate*
ncreased out6ow of a@ueous humor via contractionof ciliary muscle and opening of trabecular
meshwor3 Fiosis )contraction of sphincter pupillae* andcyclospasm )contraction of ciliary muscle*
5ilocarpine in emergencies is very e&ective inopening the meshwor3 into the canal of Sclemm
7rus for closed?narro= anle laucoma8 'rugs: aceta1olamide, miotics, topical bloc3er and
aproclonidine 'rugs are used only to terminate the attac3. ut
surgical or laser iridotomy is the de
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Antipar3insonian dugs
ANTI)AR@IN1SNIAN 7R0>S /+ASSII/ATI1N8
. 'rugs a&ecting brain do&amineric s*stem)a* 'opamine precursor: "evodopa )B8dopa*)b* 5eripheral decarbo!ylase inhibitors: arbidopa,ensera1ide.)c* 'opaminergic agonists: romocriptine,
Ropinirole, 5ramipe!ole)d* FA48 inhibitor: Selegiline)e* 4FT inhibitors: %ntacapone, Tolcapone)f* 'opamine facilitator: Amantadine.
. 'rugs a&ecting brain cholineric s*stem)a* entral anticholinergics: Trihe!yphenidyl)en1he!ol*, 5rocyclidine, iperiden.)b* Antihistaminics:4rphenadrine, 5rometha1ine.
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Dru& !herap%
Dopamine and !%rosine are not used +or ,D therap%
Dopamine doesn-t cross the blood brain barrier.
u&e amount o+ t%rosine shuts o++ rate limitin&
enz%me t%rosine h%dro"%lase that normall% conerts
t%rosine to dopamine
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/0dopa therap% +or ,D
,harmacokinetics
/eodopa is absorbed +rom the duodenum b% the
same process that absorbs neutral amino acids.
Dietar% amino acids compete ith leodopa and can
reduce the dru&-s absorption and transport into thebrain.
/eodopa is metabolized b% to patha%s. t is
conerted to dopamine b% /0aromatic amino acid
decarbo"%lase (/D)and it is metabolized to 3040meth%ldopa (345D) b% catechol40meth%ltrans+erase
(C45!).
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6++ects o+ / Dopa on Cardioascular $%stem
!he cardioascular e++ects are cardiac stimulation due to
beta adrener&ic e++ect on heart
tolerance to this e++ect in seeral eeks
treat ith propranolol to block cardiac stimulation
e++ects
5ust be care+ul in treatment o+ elderl% as most ill hae
underl%in& cardioascular problems can cause transient
tach%cardia cardiac arrh%thmias and h%pertension
n some indiiduals l dopa produces orthostatich%potension
tolerance ill deelop ithin +e eeks
$id 6++ t + / D
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$ide 6++ects o+ / Dopa
$ome are irreersible and dose dependent
6arl% in therap% 789 o+ patients hae nausea and omitin&due to chemoreceptor tri&&er zone stimulation
389 o+ patients hae orthostatic h%potension so care+ull%re&ulate dose
Cardiac arrh%thmia +rom stimulation o+ adrener&ic receptors in
heart ad;ust dose +or people ith cardiac problems #89 o+ patients hae abnormal inoluntar% moements ie.
&rimacin& o+ +ace and ton&ue moements slo rithin& t%peo+ moements (not ;erk% moements) in arm and +ace this is due to hi&h dose o+ dopa (peak dose d%skinesias)
and occurs earl% in therap% at 2 to eeks best a% to handle is b% reducin& dose
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Dru& nteractions ith / Dopa
ntips%chotic dru&s0 antips%chotic dru&s blockdopamine receptor
Reserpine0reserpine depletes dopamine stora&e
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5onoamine o"idase inhibitors
$ele&iline+or !reatin& ,arkinson Disease $electiel% nhibits 5onoamine 4"idase = >hich 5etabolizes
Dopamine but Does hich 5etabolizes
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Catechol040meth%ltrans+erase (C45!)
inhibitors
!olcaponeand 6ntacaponeare to ell0studied C45!inhibitors.
ncreases the duration o+ e++ect o+ leodopa dose
Can increase peak leels o+ leodopa
$hould be taken ith carbidopa?leodopa (not e++ectieused alone)
Can be most bene+icial in treatin& @earin& o++@responses
Can reduce carbidopa?leodopa dose b% 280389 ssociated ith seere hepatoto"icit% so hepaticenz%me estimation has to be per+ormed durin& therap%.
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!reatments o+ ,D
!he belladonna alkaloids hae been replaced b%
anticholiner&ic a&ents ith more selectie central
nerous s%stem e++ect.
!hese include trihe"%phenid%l benztropine mes%late
biperiden A proc%clidine Bsed in earl% sta&es o+ the disease as an ad;uant to /0
dopa
!he% are the onl% dru&s that can proide bene+it in the
treatment o+ the dru& induced parkinsonism seen ithantips%chotic dru&s.
t di
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n antiiral dru& moderatel% e++ectie in treatin&s%mptoms o+ parkinsonism.
5echanism unclear but mi&ht be a++ectin& dopaminerelease and uptake.nta&onism at
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lzheimers disease: 5emantine
5emantine:the ne
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FS: !reatment
nter+eron beta01bis the +irst dru& to demonstrate an
abilit% to halt and een reerse the pro&ression o+
multiple sclerosis.
ts use has been shon to reduce the +reFuenc% o+
relapses and the number o+ ne lesions. ts e++ects in patients ith multiple sclerosis ma% be due
to its immunomodulatin& properties.
nter+eron beta01b increases the c%toto"icit% o+ natural
killer cells and increases the pha&oc%tic actiit% o+macropha&es.
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!reatment
!he treatment +or /$ is lar&el% s%mptomatic. $pasticit%ma% be partl% controlled ith baclo+en a G==a&onist.!he decline in muscle stren&th ma% be sloed b%&abapentin.
!he +irst dru& that has been speci+icall% approed +or usein the treatment o+ /$ is riluzole. t prolon&s the timebe+ore patients reFuire a tracheostom% and prolon&s li+eb% about 3 months. Riluzole is belieed to protect motor
neurons +rom the neuroto"ic e++ects o+ e"citator% aminoacids such as &lutamate and to preent the ano"ia0related death o+ cortical neurons.
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'epression: TypesMild Se%ere
Stable 'ysthymia /nipolar)majordepression*
Alternating yclothymia ipolar
)manic8depression*
7*sthmiais chronic depression for at least 7 years but notsevere enough for hospitali1ation+ patient is functional at
suboptimal level/*cloth*miais alternate episodes of mania and depression ofchronic duration0ni&olar disorder maor de&ression! is severe form ofdepression with impaired functioning of the individual+ suicidaltendencies+ symptoms should present at least for 7 wee3s
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SYF5T4FS
persistently sad, an!ious, or empty moods loss of pleasure in usual activities )anhedonia* feelings of helplessness, guilt, or worthlessness crying, hopelessness, or persistent pessimism fatigue or decreased energy
loss of memory, concentration, or decision8ma3ingcapability restlessness, irritability sleep disturbances change in appetite or weight physical symptoms that defy diagnosis and do not
respond to treatment )especially pain andgastrointestinal complaints*
thoughts of suicide or death, or suicide attempts poor self8image or self8esteem )as illustrated, for
e!ample, by verbal self8reproach*
% of &
'(
SI>E M /A)S> Sleep disturbance+ loss of Interest+ >uilt+loss of Energy+ depressed Mood+ loss of /oncentration+
Appetiteweight changes+ )sychomotor
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FA4S 4N T#% FARU%T
FA4 nhibitors )nonselective* 5henel1ine
Tranylcypromine
socarbo!a1idFA48 nhibitors )selective for
FA48*
Selegiline
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FA4S S'% %((%TS
Side e&ects have put FA4s in thesecond or third line of defense despitesuperior eDcacy
FA48A inhibitors interfere with
brea3down of tyramine #igh tyramine levels cause hypertensive
crisis )the -cheese e&ect0*
an be controlled with restricted dietFA4s interact with certain drugs
Serotonin syndrome )muscle rigidity, fever,sei1ures*
5ain medications and SSRs must be avoided
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TAS 4N T#% FARU%T
Amitriptyline'esipramine'o!epin
mipramineNortriptyline
5rotriptyline
Trimipramine
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TAS F%#ANSF 4( AT4N
TAs inhibitserotonin,norepinephrine, and
dopaminetransporters,slowing reupta3e
TAs also allow for
the downregulationof post8synapticreceptors
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TAS S'% %((%TS
Fuscarinic FB receptor antagonism 8anticholinergic e&ects including dry mouth,blurred vision, constipation, urinary retention andimpotence
#istamine #B receptor antagonism8 sedation
and weight gain Adrenergic receptor antagonism G tachycardia,
postural hypotension, Arrhythmigenic at to!icdoses
'irect membrane e&ects 8 reduced sei1urethreshold, arrhythmia
Serotonin 8#T7 receptor antagonism 8 weightgain )and reduced an!iety*
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Fost important SSR
luo'etine
lu%o'amine
)aro'etine
Sertraline/italo&ram
Escitalo&ram
Selective Serotonin Re upta3e
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Selective Serotonin Re8upta3enhibitors )SSR*
Fore modern )Bstdrug 6uo!etineavailable in BVJJ* and safeantidepressants
)rinci&al mechanism of action8 selecti%e inhibition of B-
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Ad%erse eDects
Relative improvement to other antidepressants )mostlymild*
>IT
nausea, vomiting, abdominal cramps,
diarrhea relatively fre@uent, higher doses=
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N4R%5N%5#RN%8'45AFN%R%/5TAU% N#T4RS )N'RS*
urrent drugs 2u&ro&ion
Fechanims of Action
Similar to SSRs and SNRs Fore potent in inhibiting dopamine Also anC89 nicotinic antagonist
Adverse e&ects "owers sei1ure threshold Suicide 'oes not cause weight gain or se!ual dysfunction
)even used to treat the two*
use: severe depression X SM1@IN>/ESSATI1N TREATMENT
=upropion 1:1
); 1
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); 1ANTI7E)RESSANTS
A"" tricyclics bloc3 the reupta3e of both N% and8#T.
SSR;s bloc3 8#T reupta3e.
SNR;s bloc3 N% reupta3e.
other cyclics have mi!ed e&ects on N% and 8#T reupta3e.
FA4;s prevent metabolism of theneurotransmitters )elevation of synaptic levels*.
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S;M)T1MS 1 MANIA
increased energy)buying, phoning, se!*
increasedgregariousness
pressured speech,tal3ativenessdecreased sleepdrun3enness
combative, dangerousbehavior
distractibilityracing thoughts
impulsive actions anddecisions
elevated mood
euphoria
grandiosity
irritabilityhostility)easily angered*AT+EAST of the follo=in and should last at least , =eeC7I>AST> 7istractibility+ Irresponsible behavior )see3s pleasurewithout regard to conse@uences+ >randiosity)increased self8esteem*+ light of ideas+ Agitation )psychomotor* and increasedgoal8directed activity+ Sleep )decreased*+ Tal3ativeness or
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/+INI/A+ );
primary therapy for mania
a narrow therapeutic window )K.J8B.7me@"+ some guides say K.Q8B.9
me@"*
absolutely necessary to monitorserum level )trough level appro!. days after initial dose*
solely eliminated by 3idney, thereforeassess patient;s 3idney function
"ithium to!icity and adverse
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"ithium G to!icity and adversereactions
Acute into'ications*m&toms8
2T: vomiting, profuse diarrhea NS: confusion, tremorata!ia,
convulsions, coma. #eart:arrhythmias, hypotension
To'icit* of lon-term thera&* Renal to!icity G the 3idneys ability to
concentrate theurine is decreasedAd%erse reactions: polyuria and polydipsia, weight
gain, 2T disturbances )vomiting, nausea, dyspepsia*,alopecia
7ru interactions: thia1ides G increased "ireabsorption into!ication
+ithium side eDects8MN1)> Movement )tremor*+ Nephrogenic diabetes insipidus+ 1#yp1thyroidism+ )regnancy problems
oronal sections
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The rostral surface of asection of brainthrough the anteriornucleus o thethalamus$mammillothalamictract$ and mammillarybodies
#ori1ontal section
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Hentral surface of ana!ial section of brainthrough the genu othe corpus callosum$head o caudatenucleus$ centromediannucleus$ and dorsalportions o the pul"inar
Normal T
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Normal T
A. Anterior #orn of the "ateralHentricle. audate Nucleus. Anterior "imb of the nternalapsule'. 5utamen and 2lobus 5allidus%. 5osterior "imb of the nternalapsule(. Third Hentricle
N l T
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Normal T
angiogram
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angiogram
Schi1ophrenia
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p Subtypes
)aranoid8 'elusions of persecution or grandeur+4ften auditory hallucinations+ 'isorgani1ed speechand behavior
/atatonic8Fotor immobility as evidenced bycatalepsy or complete stupor+ rigidity of posture+
%!treme negativism+ %cholalia or echopra!ia+alternatively can be e!cited and show e!cessive motoractivity
7isoraniFed8'isorgani1ed speech and behavior+6at a&ect+ e!plosive laughter+ poor personal
appearance 0ndiDerentiated85sychotic symptoms that doesn;t
meet criteria for paranoid, catatonic or disorgani1ed
Residual8 5revious episode, but no psychoticsymptoms+ but negative symptoms are present
Schi1ophrenia
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5ossible mechanisms 7o&amine8
'rugs that increase dopamine will enhance or producepositive psychotic symptoms
All 3nown antipsychotics drugs capable of treating positivepsychotic symptoms bloc3 the dopamine receptors
(indings of increased dopamine receptor sensitivity in
postmortem studies Serotonin8
2enes involved in serotonergic neurotransmission areimplicated in the pathogenesis of schi1ophrenia
>lutamate8
Fajor neurotransmitter in pathways 3ey to schi1ophrenicsymptoms
loc3ing the NF'A channel may produce positive andnegative psychotic symptoms identical to schi1ophrenia
Typical antipsychotics
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To!icity: %!trapyramidalsymptoms
?ithin B w3 dystonia )muscle spasm, sti&ness, oculogyric crisis* ?ithin 7 w3 a3inesia )inability to initiate movement*
?ithin C8Q w3 rigidity, tremor and brady3inesia )par3insonism*
?ithin BK w3 a3athisia )restlessness*
9 months tardive dys3inesia )long term use: tremors and spasm
of nec3, body and limbs* %ndocrineside e&ects: dopamine receptor antagonism
leading to hyperprolactinemia
Fuscarinic bloc3ing may cause dry mouth, constipation+histamine bloc3ing may cause sedation+ B8bloc3ade may
result in hypotension ?eight gain and sedation common due to #B receptor
bloc3ade
Adverse e&ects of thiorida1ine include cardioto!icity)torsades de pointes8@uinidine li3e* and retinal deposits
syndrome
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syndrome To!ic e&ect of typical antipsychotics )#aloperidol, Tri6uopera1ine,
(luphena1ine*
A rare but life8threatening reaction to a neuroleptic medication
characteri1ed by: Fental status changes
Severe muscle rigidity )board8li3e rigidity*
(ever
Autonomic instability
linical features
Treatment:
'antrolene
'opamine '7 agonists
Mental status chanes nitial symptom Agitated delirium
with confusion atatonic signs Futism )inability to
spea3* %volution to profound
encephalopathy andcoma is typical
Muscular riidit* -"ead pipe rigidity0throughout range ofmotion
Superimposed tremor 'ysarthria,
dysphagia
Autonomic instabilit* Tachycardia mostcommon
"abile blood pressure Tachypnea 'iaphoresis
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Fechanism of action: A&ect both positive and negative symptoms
8#T7A antagnoists lo1apine has very high aDnity for 8#T7A receptors+ but lowaDnity to '7 receptors and thus dissociate rapidly. So lesse!trapyramidal symptoms
Also 8#TBA agonists )1iprasidone, @uetiapine, clo1paine* thatwould increase dopamine release )prefrontal corte!* and reduce
glutamate release linical uses
Schi1ophrenia
ipolar disorder
An!iety disorder
'epression and mania Adverse e&ects
lo1apineolan1apine has high aDnity for serotonin receptors+ maycause weight gain
lo1apine causes life8threatening agranulocytosis and sei1ure+patients on olan1apine may develop diabetes
Neurotransmitter changes
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7IS1R7ER NE0R1TRANSMITTER
/ES
5ar3insons disease 'ecreased dopamine,ncreased Ach andSerotonin
#untington;s disease 'ecreased Ach and
2AA, ncreaseddopamine
Schi1ophrenia ncreased dopamine
Al1heimer;s 'ecreased Ach
'epression 'ecreased serotonin,
norepinephrine anddopamine
An!iety ncreasednorepinephrine,'ecreased 2AA andserotonin
Neuromuscular8bloc3ingd
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drugs /sed for muscle paralysis in surgery or mechanical ventilation.
Selective for motor )vs . autonomic* nicotinic receptor
Types of neuromuscular8bloc3ing drugs 'epolari1ing: 'epolari1es the motor8end plate. %.g., succinyl choline
Non8depolari1ing: competitive antagonists at the Ah receptor. %.g.,Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium ,rocuronium
Re%ersal of blocCade 7e&olariFin8
'uring phase )depolari1ing phase*, they cause muscular fasciculations )muscletwitches* while they are depolari1ing the muscle
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Addiction pathway
The basic addiction pathway in the brain is adopamine pathway
Food8altering drugs share a remar3able ability toelevate brain dopamine levels
t is synthesi1ed by neurons in the ventraltegmental area, and released onto neurons in thenucleus accumbens and prefrontal corte!
The series of projections from: B* prefrontalcorte! to 7* nucleus accumbens to C* ventral
pallidum is a
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WernicCeGs ence&halo&ath*
G 'egenerative brain disease
G Fental confusionG 'ue to thiamine de
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%&ects on fetal e!posure in utero )(etal alcoholsyndrome*
Small stature, underweight for length Small brain, facial dysmorphia, small mid8face, smooth
philtrum )vertical groove in median part of upper lip*,thin vermilion, small palpebral
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p 5sychostimulants
Fechanism: releases hih le%els of
do&amine binding to the pre8synaptic membrane
of dopaminergic neurones andinducing the 'A release
interacting with dopamine containingsynaptic vesicles
binding to monoamine o!idase indopaminergic neurones and preventingthe degradation of dopamine, leavingfree dopamine in the nerve terminal
hronic abuse may causee!tensive tooth decay )called
meth8mouth* and a 5ar3inson8li3e movement disorder
ndications A'#'
Narcolepsy
Short term weight loss
%cstacy
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'erivative of amphetamine
chemical name is C,98
methylenedio!ymethamphetamine )F'FA* Fechanism: serotonin pathways are thevulnerable pathways+ bloc3s serotonintransporters+ After long8term or repeateduse, %cstasy causes degeneration ofserotonin nerve terminals
Acute e&ects of ecstacy #eightened perceptions )neocorte!*
Reduced appetite )hypothalamus*
Stimulation )asal ganglia*
%levated mood )Amygdala*
louded thin3ing )short8term e&ect+ neocorte!
and hippocampus* Femory impairment )long8term+ neocorte! and
hippocampus*
Sometimes, muscle spasms and jaw8clenchingare due to ecstasys action at the motor neuronsin the spinal cord
Serotoninneuron
Serotonin
#eadache MI>RAINE8
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MI>RAINE8
enign and recurrent syndrome of headache,nausea and vomiting and varying neurologicalde
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/+0STER
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TENSI1N
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Be able to draw this pattern. -RandyTravis 'rin3s old eer0
The origin of the brachialple!us is from ventral rami./nfortunately, the term-roots0 has been used. Thebrachial ple!us does N4Tarisefrom dorsal or ventral roots,nor from the dorsal rami.
2ranches of the cords
Lateral cord branches:" t l t f di
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"ateral root of medianN),Q,O*"ateral pectoral N
),Q,O*Fusculocutaneous N),Q,O*
Medial cord branches: All Ms!Fedial root of median N)J,TB*Fedial pectoral N )J,TB*Fedial cutaneous N of arm )TB* and
forearm )J,TB*
"osterior cordbranches:0+TRA08/pper subscapularnr),Q*+8"ower subscapularnr),Q*T8Thoracodorsalnr)Q,O,J*R8Radial nr),Q,O,J,TB*A8A!illary nr),Q*
"ong thoracic nerve
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Subclavian v., a.
at. thoracic a.
rratus ant. m.s B8J
tracts, secures and rotates scapula
Subscapularismuscle
"ong thoracic n. ),Q,O*7escends behind the roots
Runs alon the Serratus anteriorsu&erKciall*7urin a mastectom*-it could becut accidentall* res#lting in$inged scap#la or Angel scap#laSerratus anterior =ill no loner
hold the sca&ula in &lace
WINGING OF SCAPULAScalenus ant.
calenus med.
0&&er TrunC +esion of the 2rachial )le'usSite of +esion:
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Site of +esion:Tearing of upper trun3 orits roots.
/sually occurs pro!imal tothe branch point of thesuprascapular n. but distalto the branch point of thelong thoracic n. and dorsalscapular n
/ause of +esion:Trauma incurred in
infants durincom&licated deli%er*+
n adults, by %iolent fallson side of head and
shoulder(
ErbLs )als*H Erb-7uchenne )aral*si
0&&er TrunC +esion of the 2rachial )le'usN I l d
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Ner%es In%ol%ed:
A!illary n.Suprascapular n.Fusculocutaneous n."ateral cutaneous n.of forearm
+oss of motorfunction:
Fuscles of the &ro'imal
u&&er limb innervated bythe nerves listed above)deltoid, teres minor,supraspinatus,infraspinatus, biceps
brachii, coracobrachialis,
+oss of Sensation:0&&er TrunC +esion of the 2rachial )le'us
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+oss of Sensation:5osterolateral aspect ofthe superior part of the
arm, lateral aspect ofthe forearm
)osition of the +imb8
Arm: %!tended,adducted and rotatedmedially.(orearm: %!tendedand pronated.IThis position of thelimb is often describedas Mhead =aiterLs ti&Mposition.
"ateralcutaneous n ofarm )froma!illary*
"ateralcutaneous n offorearm )frommusculocutaneous*
Anterior%ie=
A'illar* ner%e inur*Site of +esion:
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Site of +esion:/sually in the portion of nervewhich is adjacent to the surgicalnec% o the humerus./ause of +esion:(racture at surgical nec3 ofhumerus. 5osterior dislocation of
the head of the humerus+oss of Muscle unction:'eltoid and teres minor mm.+oss of Sensation:
S3in on the posterolateral aspect ofthe superior portion of the arm.)osition of the +imb:
Arm: Adducted )loss ofabduction at shoulder joint*
(orearm, ?rist, #and: No e&ect
"ateralcutaneous n ofarm )froma!illary*
)osterior%ie=
+o=er TrunC +esion of the 2rachial )le'us
Also called @lum&Ce
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so ca ed u & e)aral*sis
Site of +esion:Tearing of lower trun3 or itsroots.
/ause of +esion:Trauma incurred in infantdurin com&licateddeli%er* often in breech&resentationswhere arm iscarried over the head.
n adults, fallin =ith thearm outstretched o%erthe head )as in falling froma ladder and attempting tocatch oneself by one hand*
from a tumor at the ape!
+o=er TrunC +esion of the 2rachial )le'us
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Ner%es in%ol%ed:/lnar,
medial cutaneous n of arm,medial cutaneous n offorearm.
+oss of motor
function:Fuscles of the distal u&&erlimbthat are innervated byulnar nerve, i.e., 6e!or carpiulnaris, medial B7 of 6e!or
digitorum profundus m.,medial two lumbrical mm.,all interosseous mm.,adductor pollicis m.
Also called @lum&Ce)aral*sis+o=er TrunC +esion of the 2rachial )le'us
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+oss of sensation:?idespread loss of sensation on
the medial aspect of the arm)medial cutaneous nerve ofarm*,The medial aspect of forearm)medial cutaneous nerve of
forearm*,wrist and hand )cutaneousdistribution of the ulnar nerve*.
)osition of the +imb8
Arm8 No changeorearm8 No change
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Site of +esion8/sually at the wrist
where the median nervepasses through the carpaltunnel )carpal tunnelsyndrome*.
/ause of +esion85ressure on the nerve inthe carpal tunnel, most
often related to nonspeci
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Ape hand
Fedian n
unction8"ateral two lumbrical
mm.+ All thenarmuscles: 6e!or pollicisbrevis m., abductorpollicis brevis m.,opponens pollicis m.
+oss of Sensation8"ateral aspect of thepalm and lateral C B7
digits )loss of sensationin thumb and inde!
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Site of +esion8B* most commonly at the
level of the elbow due tocompression of the nervein the roo%e for theulnar ner%e, or afracture of the mediale&icond*le of thehumerus or a lacerationat this location+
7* occasionally the ulnarnerve is lesioned at the=rist due to alaceration.
0lnar ner%e inur*+oss of muscle function8
i di l i d l i
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)B*Lesion at medial epicondyle )7*Lesion at%rist
Fedial two heads of 6e!or Fedial two lumbricals,digitorum profundus, 6e!or all interossei,
adductorcarpi ulnaris, medial two pollicis and mm. of
lumbricals, all interossei hypothenar eminence.adductor pollicis, mm ofhypothenar eminence.
0lnar ner%e inur*+oss of sensor* function8&1'Lesion at medial epicondyle )7*Lesion at%rist
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/lnar n
"oss of sensation for medial "oss of sensation overthe
aspect of hand including the hypothenar eminenceand
hypothenar eminence and palmar surface of themedial B B7 digits 8 both medial B B7 digits
)dorsaldorsally and ventrally surfaces of these digits
are una&ected because thedorsal branch of the ulnar
nerve is spared*
0lnar ner%e inur*
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)osition of the +imb8)B*Lesion at medial epicondyle )7*Lesion at
%rist#and slightly abducted. nability to abduct
and adductnability to abduct and adduct digits 7 8 ,
digits 7 8 , inability to adduct inability toadduct the thumb the thumb
Radial ner%e inur*Site of +esion8
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/sually at the mid8shaft of the
humerus. hronic pressure in thea!illa e.g. rutch use
/ause of lesion8
(racture of mid8shaft of thehumerus+ pressure on the nervecaused by crutches.
+oss of muscle function8
%!tensors of the wrist and
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5osterior forearm+ dorsum of the hand on the radialside, including the dorsum of the lateral C B7 digits
)e!cept over the distal phalan!*. The s3in on thedorsum of the hand, overlying the interval between theBst and 7nd metacarpals, can be tested in evaluatingthe function of the radial nerve.
5osteriorcutaneous
n offorearm)fromradialnerve*Superi
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cannot be e!tended. #owever, this doesnot mean that an object can be gripped
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/ommon ibular )eroneal!Ner%e Inur* 8
njury generally occurs as thenerve wraps around the lateralaspect of the
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Su&erior >luteal
Ner%e Inur* 8njury to this nerveleads to a -gluteusmedius limp0 due to thegluteus minimus and
medius beingdenervated.
The person leans away
from the unsupportedside )i.e., leans towardthe side of the injury*when wal3ing+ this is a-5ositive Trendelenberg0
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T