Medicine exam 2013/14
Course title:
5.2 Nervesystemet og bevægeapparatet II (Neurology II)
Programme:
Bachelor in education
Semester:
5th semester
Exam date:
17-01-2014
Time:
09:00-13:00
Evaluation form
7-point scale
Important information:
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Remember to bring your student identification card
Remember to put your student number – not your name and cpr no – on all sheets that
you hand in for evaluation (if written exam)
Remember to hand in the assignment if you leave the exam before it has ended
No written aid is allowed
Your paper must be handed in on paper in hand written form
Quicktionary pen is allowed (no other electronic devices are allowed)
The study board/the university cannot be held liable if any problems should occur
regarding the electronic aid during the examination
It will be considered cheating or attempting to cheat if the technical equipment of the
student is communicating or trying to communicate with other equipment not relevant to
the exam, without an explicit permission. Before the beginning of the exam, the student
should make sure that all communication devices in the equipment at the exam are turned
off.
Communication is not allowed
Answers both in Danish and English allowed.
Point system (7-scale, max: 225 Points, 60%: passed (135 P)):
Passed: 12 (225-209); 10 (208,5-190,5); 7 (190-172); 4 (171,5-153,5); 2 (153-135);
Failed: 0 (134,5-68); -3 (67,5-0)
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1. Dementia (20 Points)
a) Give a brief definition for dementia and an overview of its classification (7 Points).
b) Describe the amyloid and vascular hypothesis. (10 Points)
c) What score on the “MMSE” as an easy test for cognitive impairment represents the normal
range? Name one treatment option (substance class + example) (3 P points)
a) Main types: Neurodegenerative/progressive: Alzheimer’s disease/Vascular
dementia/Frontotemporal dementia/Dementia with lewy bodies/ parkinson’s disease with
dementia; Non-neurodegenerative/non-progressive: depression/hydrocephalus/space-occupying
lesions/ metabolic diseases/epilepsy
Def.: Dementia is a syndrome in which there is deterioration in memory, thinking, behavior and the
ability to perform everyday activities; Impaired cognitive functions
b) Pathophysiology: AD: Extracellular amyloid plaques + Intracellular neurofibrillary tangles;
Shrinkage of brain tissue; progression: mild-moderate-severe; amyloid hypothesis (mutations in
APP/PS1/PS2 genes; increased Abeta42 production+accumulation; Abeta42 oligomerizes+plaque
depositions; activation of microglia+astrocytes/progressive synaptic and neuritic injury; altered
neuronal ionic homeostasis/oxidative injury; altered kinase/phosphatase activities; wide spread
neuronal/neuritic dysfunction and cell death/transmitter deficits); vascular hypothesis (Vascular
risk factors (e.g., hypertension, diabetes, obesity, cardiac disease) and/or an initial vascular damage
mediated by a cerebrovascular disorder (e.g., ischemia, stroke) lead to brain hypoperfusion
(oligemia) and/or blood–brain barrier (BBB) dysfunction, which is associated with a diminished
brain capillary flow/hypoxia and accumulation of multiple neurotoxins in brain, respectively, that
can impact neuronal function contributing to the development of neurodegenerative changes and
cognitive decline. In a parallel pathway, BBB dysfunction and hypoperfusion/hypoxia can reduce
amyloid beta peptide (Ab) vascular clearance across the BBB and increase Ab production from Abprecursor protein (APP), respectively, causing Ab accumulation in brain. Elevated Ab levels lead to
formation of neurotoxic Ab oligomers, causing neuronal dysfunction, on the one hand, and selfaggregation, on the other, which leads to self-propagation of Ab-mediated brain disorder and the
development of cerebral b-amyloidosis. According to the vascular hypothesis, a pathogenic tau
phosphorylation in neurons and the development of tau-related pathology including neurofibrillary
tanglesmay be triggered independently or simultaneously by a hypoperfusion/hypoxia insult and/or
direct Ab neurotoxicity.
c) MMSE / Mini Mental State Examination:
24-30: “normal range”
20-23: mild cognitive impairment
10-19: middle stage
0-9: late stage
Treatment: cholinesterase inhibitors (donezepil, galantamin, rivastigmin); glutamate receptor
antagonists (memantin)
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2. Cerebrovascular (36 P)
a) Describe the main (core) structures of the circulus anteriosus cerebri/circle of Willis
(recommended: drawing+labels). (8 P)
b) Elaborate on the concept of raised intracranial pressure (including the different stages) and
briefly summarize early clinical signs of neurological deterioration in that context. (9 P)
c) Give a schematic overview of different types of cerebrovascular diseases (apoplexia cerebri). (10
P)
d) Give an overview of head injuries (categories + short description/explanation). (9 P)
a)
b) increased IP may result from - increase in intracranial content, e.g. tumor growth/ edema/
excess CSF/ hemorrhage; a rise in IP necessitates an equal reduction in volume of other contents
(Monro-Kellie doctrine); most readily displaced content of cranium is CSF
Stage1: if IP remains high after CSF displacement, cerebral blood volume is altered
Stage2: IP begins to compromise neuronal oxygenation, and systemic arterial vasoconstriction
occurs in an attempt to elevate systemic blood pressure to overcome increased IP
Stage3: loss of autoregulation, the compensatory alteration in diameter of intracranial blood
vessels designed to maintain a constant blood flow during changes in cerebral perfusion pressure.
brain volume further enhanced with progressively increased IP. Severe hypoxia and acidosis.
Stage 4: brain tissue shifts (herniates) from the compartment of greater pressure to a compartment
of lesser pressure
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c)
d) Simple concussion - transient loss of consciousness followed by complete recovery. Short period
of amnesia is often related to loss of consciousness.
Brain contusion refers - brain damage with prolonged coma, amnesia and focal signs. Patients
often suffer from chronic impairment of higher cerebral functions and hemiparesis (Post-traumatic
epilepsy).
Extradural or epidural haematoma: rupture of the middle meningeal artery due to a skull fracture
or by tearing of dural veins to the sagittal sinus. Skull fracture sometimes accompanied by CSF loss
(eg, rhinorrhoea and otorrhoea). Following head injury with a period of unconsciousness, patient
may appear in a good condition, but suddenly he looses consciousness or develops hemiplegia.
Subdural haematoma: Accumulation of blood in subdural space caused by venous bleeding. The
cause is head injury with latency between the event and the symptoms (headache, confusion,
stupor, coma, delirium, hemiparesis, epilepsy etc).
Subarachnoid haemorrhage: Spontaneous arterial bleeding into the subarachnoid space. The
clinical picture can be that of delirium. Neurosurgical closure of the aneurysm is sometimes
possible.
Intracranial mass lesions: Located supratentorially (above the tentorium cerebelli) can compress
the brain towards the tentorium as to block the upward flow of CSF and thus its absorption. Such
mass lesions are brain tumors, encephalitis, meningitis, haemorrhages, aneurysms, brain abscesses,
and the effect is similar to the effect of brain contusion just analysed.
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3. Cranial nerves (40 P)
a) Name the cranial nerves VII, VIII and IX and give a very short description of their component
fibers (mixed, purely sensory/motor, etc.), functions and structures that are innervated. (12 P)
b) Which muscles are innervated by the cranial nerves III, IV and VI regarding eye movement and
what is their function? (6 P)
c) Describe schematically (draw a diagram) on the neural pathways for vision (including visual
fields).
Add into that drawing which different visual pathway defects may occur with right-sided lesions.
(10 P)
d) Describe the anatomy of the retina (cell types). (5 P)
e) Briefly describe 3 tests for the examination of hearing impairments. (5 P)
f) How do you test for damage of the first cranial nerve? (2 P)
a) VII/N. facialis; mixed; sensory: anterior 2/3 tongue; secretomotor: salivary+lacrimal; motor: facial
muscles (expression)/digastric (hyoid bone)/stylohyoid (tongue elevation)/stapedius (stapes: sound
amplitude control)
VIII/N. vestibulocochlearis: sensory; vestibular: balance+equilibrium; cochlear: hearing
IX/N. glossopharyngeus; mixed; sensory: posterior 1/3 tongue, palatine tonsils; secretomotor:
parotid gland; motor: stylopharyngeus (larynx elevation; pharynx elevation+dilation); swallowing
b) M. rectus superior: eye looks up (CN III/ N. occulomotorius)
M. rectus medialis: eye looks medially (adduction) (CN III/ N. occulomotorius)
M. rectus inferior: eye looks down (CN III/ N. occulomotorius)
M. obliquus inferior: eye rolls, looks up, laterally (CN III/ N. occulomotorius)
M. obliquus superior: eye rolls, looks down, laterally (CN IV/ N. trochlearis)
M. rectus lateralis: eye looks laterally (abduction) (CN VI/N. abducens)
c)
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d)
e) Weber test: In the Weber test a tuning fork (256 or 512 Hz) is struck and stem of fork is placed
on top of the patient's skull - equal distance from the patient's ears, in the middle of the forehead equal distance from the patient's ears or above the upper lip over the teeth. The patient is asked to
report in which ear the sound is heard louder. A patient with a unilateral (one-sided) conductive
hearing loss would hear the tuning fork loudest in the affected ear. This is because the conduction
problem masks the ambient noise of the room, whilst the well-functioning inner ear picks the
sound up via the bones of the skull causing it to be perceived as a quieter sound in the unaffected
ear. Another theory, however, is based on the occlusion effect described by Tonndorf et al in 1966.
Lower frequency sounds (as made by the 512 Hz fork) that are transferred through the bone to the
ear canal escapes from the canal. If an occlusion is present, the sound cannot escape and appears
louder on the ear with the conductive hearing loss.
Rinne test: The Rinne test is performed by placing a vibrating tuning fork (512 or 256 Hz) initially on
the mastoid process until sound is no longer heard, the fork is then immediately placed just outside
the ear. Normally, the sound is audible at the ear. Air conduction uses the apparatus of the ear
(pinna, eardrum and ossicles) to amplify and direct the sound whereas bone conduction bypasses
some or all of these and allows the sound to be transmitted directly to the inner ear albeit at a
reduced volume, or via the bones of the skull to the opposite ear. In a normal ear, air conduction
(AC) is better than bone conduction (BC) AC > BC, and this is called a positive Rinne. In conductive
hearing loss, bone conduction is better than air BC > AC, a negative Rinne. In sensorineural hearing
loss, bone conduction and air conduction are both equally depreciated, maintaining the relative
difference of AC > BC, a positive Rinne.
Audiogramm: An audiogram is a standard way of representing a person's hearing loss. Most
audiograms cover the limited range 100Hz to 8000Hz (8kHz) which is most important for clear
understanding of speech, and they plot the threshold of hearing relative to a standardized curve
that represents 'normal' hearing, in dBHL.
e) sniff aromatic substances: e.g. vanilla, cinnamon, coffee
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4. Joint diseases (20 P)
a) Briefly describe central pathophysiological aspects of osteoarthritis and rheumatoid arthritis. (10
P)
b) Describe 3 groups of drugs used in musculoskeletal disorders (including examples) and
summarize (essence) the mode of action for these groups. (6 P)
c) What is the key pathophysiological feature of crystal arthropathy? Give 4 treatment options. (4
P)
a) osteoarthritis: OA most common and most frequent joint disorder; common age-related
disorder of synovial joints (begins in 3rd decade, peaks in 5th and 6th); Characterized by local area
of loss and damage of articular cartilage (progressive; erosion, eburnation), new bone formation of
joint margins (osteophytosis), subchondral bone changes, variable degrees of mild synovitis,
thickening of joint capsule; on hands: Bouchard + Heberden nodes (PIP vs. DIP); Pathology centers
on load-bearing areas. OA affects mostly the cartilage of hand, knee, hip and spine;
Multi-factorial disease involving environmental-lifestyle factors and genetics involves low-grade
inflammation, calcification of articular cartilage, genetic alterations, metabolic disorders;
inflammatory mediators: TNF; IL (1beta, 6, 8, 15, 17, 21), PGE2, Substance P, NGF, EGF, VEGF, FGF-2
signaling mediators: NFkB, ERKa/2, p38, JNK, PKC delta, TLRs, beta-catenin, Gli1, Ptch, HHIP, HIF2alpha, iNOS, RUNX2; Proteases: MMP (1, 3, 9, 13), ADAMTS (4, 5), TACE
Risk factors: Trauma, sprains, strains, joint dislocation, fractures, long-term mechanical stress
(athletics, ballet) or repetitive physical tasks, obesity, inflammation in joint structures (production
of enzymes digesting cartilage), joint instability due to damage to supporting structures (e.g. joint
capsule, ligaments, tendons), Neurological disorders (diabetic neuropathy, Charcot neuropathic
joint) with diminished or lost pain and proprioception reflexes; tendency for abnormal movement,
positioning or weight-bearing, congenital or acquired deformities, hematologic (hemophilia) or
endocrine disorders (hyperparathyroidism), drugs (colchicin, steroids, indomethacin);
Pathophysiology: primary defect/loss of articular cartilage; → early stage: articular cartilage loses
glistening appearance; → disease progress: fibrillation (surface areas of articular cartilage flakes off
and deep layers develop longitudinal fissures); → cartilage becomes thin or even absent, bone
unprotected (subchondral bone); → subchondral bone becomes sclerotic (dense & hard); → cyst
development within subchondral bone; pressure builds in cysts; until cystic contents are forced into
synovial cavity damaging more; articulate cartilage; → with erosion of articulate cartilage: cartilagecoated osteophytes may grow; outward from underlying bone and change bone contours and joint
anatomy;→ joint capsule thickens
clinical manifestation: pain and stiffness in one more joints (usage-related pain relieved with rest);
crunching feeling/sound of bone rubbing on bone;
Rheumatoid arthritis: Systemic inflammatory autoimmune disease targeting multiple joints; First
joint tissue to be affected: synovia; Immunoregulatory cytokines (interleukins, B-Cells, matrix
metalloproteinase) contribute to joint damage; Inflammation spreads to articulate cartilage, fibrous
joint capsule, surrounding ligaments and tendons causing pain, joint deformity and loss of function;
Most commonly affected: fingers, wrist, feet, ellbows, ankles, knees; (also: shoulders, hips, cervical
spine as well as tissues of lungs, heart, kidney and skin); RA affects 1-2 % of adults, develops most
often in women (ratio 3:1); RA frequency increases from 3rd decade on, affecting ≥5 %; RA can also
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cause fever, malaise, rash, lymph node or spleen enlargement, Raynaud phenomenon (transient
lack of circulation to toes & fingertips); Rheumatoid factors/RF: immunglobulin antibodies for IgM
& IgG, occasionally IgA;
Pathophysiology: Cartilage damage in RA is due to several processes: 1. Activation of CD4 T-helper
cells (and other cells in synovial fluid) promoting cytokine release & activating B-lymphocytes 2.
Recruitment & retention of inflammatory cells in the joint sublining region
3. Vicious cycle of altered cytokine & signal transduction pathways 4. Possible immune complex
deposition and resultant inflammatory molecule release 5. RANKL (receptor-activator of NF-kB
ligand) -release and osteoclast activation 6. Angiogenesis, or growth of new blood vessels in the
synovium; Inflammation causes hemorrhage, coagulation and fibrin deposition in synovial
membrane, intracellular matrix and synovial fluid. Pannus: fibrin develops into granulation tissue
over synovium, composed of several different cells (especially: osteoclasts and synovial fibroblasts);
Evidence includes: Presence of androgen & estrogen receptors/High concentrations of biologically
active steroids/Key enzymes of steroid metabolism/Significant changes of androgen / estrogen
ratio;
RA-evaluation by: Physical examination, roentgenography, serologic tests for RF, circulating
immune complexes;
possible complications: Carpal tunnel syndrome; Baker‘s cyst; Vasculitis; Sjögren‘s syndrome;
Peripheral neuropathy; Cardiac and pulmonary involvement; Felty‘s syndrome; Subcutaneous
nodules;
typical manifestations on hands: subcutaneous nodules + ulnar drift
b) Bisphosphonates: Pyrophosphate analogues (enzyme-resistant), inhibit bone resorption mainly
by acting on osteoclasts; After administration: → bound to bone minerals in the matrix; → released
slowly as bone is resorbed (osteoclasts); → thus osteoclasts exposed to high drug concentrations;
(Alendronate, risedronate, ibandronate); osteoporosis
estrogens: + SERM (selective estrogen receptor modulator; raloxifene; dose-dependent effect on:
↑ osteoblast activity/↓ osteoclast activity); osteoporosis
NSAID: inhibits prostaglandin biosynthesis → anti-inflammatory, analgesic and antipyretic effect
(Acetylsalicylic acid (aspirin), ibuprofen, diclofenac, naproxen)
DMARDS: Sulfazalazine (IgA and IgM rheumatoid factor production decreased suppression of T cell
responses, inhibition of in vitro B cell proliferation); gold (sodium aurothiomalate/i.m.;
auranofin/oral; Alter morphology and functional capabilities of macrophages → monocyte
chemotactic factor-1, IL-1, IL-1β & vascular endothelial growth factor ↓; i.m. gold alters lysosomal
enzyme activity, ↓ histamine release, inactivation of first component of complement system ↓
phagocytic activity of leucocytes; Oral gold: ↓ PGE2 and leukotriene B4 release);
immunosuppressants: methotrexate (Folic acid antagonist, cytotoxic and immunosuppressant; ↓
purine metabolism enzymes/→ accumulation of adenosine; ↓ T cell activation/suppression of
intercellular adhesion molecule expression); azathioprine (Metabolized to mercaptopurine →
thioguanine: purine analogue, ↓ DNA synthesis; Both cell-mediated & antibody-mediated immune
reactions are depressed → inhibits B cell and T cell function, Ig production, IL-2 secretion)
c) key pathological feature: Characterized by hyperuricemia (high levels of uric acid in body fluids
e.g. synovium, blood; by-product of protein metabolism; overproduction/underexcretion of uric
acid), recurrent attacks of monoarticular arthritis (single joint), tophi deposits in and around the
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joints, renal disease (involving glomerular, tubular and interstitial tissues and blood vessels),
formation of renal stone;
Other factors include age, excessive alcohol consumption, genetic predisposition; (X-linked
HGPRT/hypoxanthine-guanine phosphoribosyltransferase), obesity, certain drugs (especially
thiazides), lead toxicity;
Classical gouty arthritis: monosodium urate crystals form and cause inflammation
medications: NSAIDS/Xanthine oxidase inhibitors (allopurinol, febuxostat)/NSAIDS-intolerants:
Colchicine/Hydrocortisone injection into the joint for pain relief/Interleukin-1 antagonists
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5. Mixed topics (34 P)
a) Define the term MAC and briefly elaborate on its meaning (give also an example for older and
more recent inhalation anaesthetics). (6 P)
b) Summarize main groups of muscle relaxants/neuromuscular blockers (give 3 examples). (10 P)
c) What is the chemical basis for local anaesthetics (functional groups). What is their mode of
action? Give 1 example each according to the chemical characteristics. Which nerve fiber types are
affected first. ( 8 P)
d) What does the term “BOLD-signal” stand for, with which imaging technique is it recorded and
what is the physiological basis for it? Describe briefly the meaning of a T1 and a T2 signal. (8 P)
e) Elaborate on the temporal and spatial resolution of imaging techniques EEG and MRI (pro’s vs.
cons); 2 P
a) minimal alveolar concentration; anaesthetic potency: anaesthetic concentration to abolish
response to surgical incision in 50 % of subjects; lipid solubility inversely proportional to MAC;
Older: ether/nitrous oxide; newer: e.g. enflurane, isoflurane, sevoflurane, desflurane
b) pre-synaptic (cholin re-uptake (hemicholinium, vesamicol); acetylcholine release (streptomycin,
botulinumtoxin)) vs. post-synaptic (acetylcholine receptors; continuous depolarization of the end
plate; inhibition of electro-mechanical coupling);
depolarizing: succinylcholine (suxamethonium)
non-depolarizing (curare-type):
short-acting: mivacurium, rapacuronium
intermediate-acting: atracurium, cisatracurium, rocuronium, vecuronium
long-acting: alcuronium, doxacurium, gallamine, metocurine, pancuronium, pipecuronium, dtubocurarine
c) Lipophilic & aromatic part linked via ester or amide bond to basic amine side-chain;
Hydrophobic/no-use-dependance
Hydrophilic/use-dependance
Esther-type: Cocaine, procaine, tetracaine,
Amide-type: lidocaine, bupivacaine, prilocaine
unmyelinated>>heavily myelinated (C>B>Adelta>Abeta/gamma….)
d)BLOOD OXYGENATION LEVEL DETECTION; fMRI;
oxygenated hemoglobin: diamagnetic
de-oxygenated hemoglobin: paramagnetic
blood oxygenation levels in neuronal tissue elevated with neuronal activity (higher perfusion/bigger
singal)
T1: vertical magnetization curve (recovery)
T2: horizontal magnetization curve (decay)
different T-constant values for different tissues (fat, grey matter, white matter, CSF)
e) EEG: good temporal, bad spatial resolution
MRI: vice versa
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6. Upper extremities (40)
a) Describe how nerves from the brachial plexus starts from the columna vertebralis, divides and
forms the principal nerves of the upper extremities (schematic). (14 P)
b) Describe the underlying pathology of the “hands of benediction”, the “claw-finger” and the
“bottleneck” signs. (12 P)
c) What are the main structures of the carpal tunnel and what are the typical effects of a carpal
tunnel syndrome? (10 P)
d) Name the muscles of the deep and superficial wrist extensors and their innervations. Name the
superficial and deep wrist flexor muscles. (14 P)
a)
b) claw hand: N. ulnaris lesion: Characteristic feature is a ”claw hand” - loss of the M. interossei
causes the fingers to be hyperextended at the MCP joints. Plus thumb is hyperextended due to the
loss of M. Adductor pollicis;
Proximal lesion: Traumatic lesions usually occurring at the elbow joint due to the exposed position
of the nerve in the Sulcus n. ulnaris, or articular injuries due to fractures. Claw hand and sensory
disturbances.
Distal N. ulnaris lesion: Compression of the deep branch of the N. Ulnaris in the palm due to chronic
pressure (e.g. tools). Claw hand with no sensory disturbances.
Hand of benediction/bottle sign: N. medianus lesion;
Proximal medianus lesion: Fracture or dislocation of the elbow joint/Hand of Benediction – when
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fist closure is attempted, with incomplete pronation, loss of thumb opposition, impaired grasping
ability, atrophy of the thenar muscles + sensory disturbances; Positive ”Bottle Sign” – fingers and
thumb cannot close fully around a cylindrical object due to weakness of the M. abductor pollicis
brevis
Distal medianis lesion: Superficial location makes it venerable to cuts and lacerations. Chronic
compression in the Canalis Carpi (Carpal Tunnel Syndrome). Hand of Benediction is not present.
Initial signs consist of sensory disturbances (parasthesia and dysasthesia) chiefly affecting the tips
of the index and middle fingers and thumb. Chronic or severe damage leads to motor deficits
involving the thenar muscles and positive bottle sign.
c) carpal tunnel: Fibro-osseus structure; Floor is proximal carpal bones; Roof is transverse carpal
ligament; Tunnel contains 10 structures: N. medianus, flexor pollicis longus (1 tendon), flexor
digitorum superficialis (4 tendons), flexor digitorum profundus (4 tendons)
CPS: sensory disturbances (parasthesia and dysasthesia), pain, motor deficits involving the thenar
muscles and positive bottle sign.
d) Wrist extensors (innervated by radial nerves)
Superficial: Extensor carpi radialis brevis/longus, Extensor carpi ulnaris, Extensor digitorum,
Extensor digiti minimi
Deep: Extensor pollicus longus/brevis; Abductor pollicus longus, Extensor indicis, Supinator
Wrist flexors:
Superficial: Flexor carpi radialis, Palmaris longus, Flexor carpi ulnaris, Flexor digitorum superficialis,
Pronator teres
Deep: Flexor digitorium profundus, Flexor pollicis longus, Pronator quadratus
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7. Lower limb (35 P)
a) Give the insertion sites, origin and innervations of 2 anterior, posterior (both superficial and
deep) and lateral leg muscles each. Name 2 passive stabilizers of the longitudinal arch. (15 P)
b) Name 4 active stabilizers of the longitudinal foot arch and 3 passive stabilizers of the hip joint
(regarding caput femoris/acetabulum). (4 P)
c) Summarize the anatomical and physiological basis for the locking/unlocking mechanism of the
knee? (10)
d) Which are the anterior thigh muscles and by which nerve(s) are they innervated? (6 P)
a)
lateral:
anterior:
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posterior superficial:
posterior deep:
2 passive stabilizers of the longitudinal arch:
Plantar aponeurosis is particularly important owing to its long lever arm;
Lig. plantare longum; Lig. calcaneonaviculare plantare
b) 4 active stabilizers of the longitudinal foot arch: Abductor halluces, Flexor hallucis brevis, Flexor
digitorum brevis, Quadratus plantae, Abductor digiti minimi
3 passive stabilizers of the hip joint: Lig. Iliofemorale, Lig. Pubofemorale, Lig. Ischiofemorale
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c) Summarize the anatomical and physiological basis for the locking mechanism of the knee?
During the last ~20° of knee extension the tibia externally rotates / femur medially rotates.
Permits standing upright with little expenditure of energy in the form of muscle contraction.
Articular surface of the medial femoral condyle is longer than the surface on the lateral femoral
condyle.
Moving into extension from a flexed position - the articular surface of lateral femoral condyle stops.
Surface for articulation still exposed on medial condyle - anterior tibial glide persists on the tibia's
medial condyle – lateral rotation.
Lateral rotation of the tibia (NWB/nonweight bearing)/medial rotation of femur (WB/weight
bearing) accompany final stages of extension.
Accommodates remainder of exposed articular surface on medial femoral condyle.
Promotes greater contact between articular surfaces of femoral and tibial condyles.
Tightens collateral and cruciate ligaments.
d) Which are the anterior thigh muscles and by which nerve(s) are they innervated?
Quadriceps femoris (Rectus femoris, Vastus medialis, Vastus lateralis, Vastus
intermedialis)/n.femoralis (L2-L4); Sartorius/n.femoralis (L2-L4)
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