Neurology clinical exam

Question 1

Differentials for upper motor neurone weakness?

Answer 1

(HIDICOT) Ischemia - stroke, spinal cord infarct Haemorrhage - subarachnoid, intracerebral Traumatic brain injury Tumor - astrocytoma, meningioma, brain metastases, spinal cord neoplasia Infection - encephalitis, PML, brain abscess Demyelination - ADEM, multiple sclerosis Hereditary spastic paraplegia Idiopathic transverse myelitis CNS vasculitis Sarcoidosis Syringomyelia Prion disease

Question 2

Signs of upper motor neurone lesion

Answer 2

Reduced power Minimal muscle wasting, Spasticity - velocity dependent increase in tone - scissor gait Clonus - more than 3 beats Hyper reflexia Upgoing plantars

Question 3

Signs of lower motor neurone lesion

Answer 3

Reduced power Muscle wasting Reduced tone Fasiculations Hypo reflexia Downgoing plantars (normal)

Question 4

Signs of myopathy

Answer 4

Reduced power Muscle wasting Normal reflexes Normal tone Downgoing plantars (normal)

Question 5

Causes of lower motor neurone weakness affecting single myotome?

Answer 5

Likely due to spinal nerve root pathology - Spinal trauma, radiculopathy or tumor

Question 6

Causes of lower motor neurone weakness affecting single peripheral nerve distribution?

Answer 6

Likely due to focal peripheral nerve pathology - Trauma, nerve entrapment, focal ischemia, peripheral nerve tumor or sarcoidosis

Question 7

Causes of lower motor neurone weakness affecting multiple peripheral nerve distributions?

Answer 7

Due to a brachial plexus lesion or mononeuritis multiplex Brachial plexus lesion - Trauma, brachial neuritis, radiation injury, tumor Mononeuritis multiplex - Vasculitis Diabetes. infection , Malignancy, Amyloidosis, sarcoidosis

Question 8

Which vasculitides can cause mononeuritis multiplex?

Answer 8

Polyateritis nodosa, EGPA, GPA, cryoglobulinemia, SLE, rheumatoid arthritis, Sjrogrens syndrome, Scleroderma, Behcet’s disease.

Question 9

Which infections can cause mononeuritis multiplex?

Answer 9

HIV, hepatitis B and C, Leprosy, Lyme disease.

Question 10

Causes of generalised lower motor neurone weakness?

Answer 10

Suggests a polyneuropathy, neuromuscular pathology or myopathy Peripheral polyneuropathy - Endocrine/nutritional, Demyelination, Vasculitis, Infection, Paraneoplastic syndrome, Multifocal motor neuropathy with conduction block, Motor neurone disease, Charcot Marie tooth, Sarcoidosis, Drugs, toxins Myopathy -

Question 11

Causes of co-existant upper and lower motor neurone weakness

Answer 11

Quite rare - main differential would be 2 seperate pathologies, also consider amyotrophic lateral sclerosis (variant of motor neurone disease affecting UMN and LMN), Cervical myelopathy, Syringomyelia

Question 12

Causes of proximal muscle weakness

Answer 12

Tends to be a muscular pathology rather than neurological in cause. Differentials: Proximal myopathy!! Neuromuscular disorder Neurological disorder

Question 13

Signs of proximal myopathy

Answer 13

Proximal muscle wasting Symmetrical proximal weakness (shoulders/hips) Trendelenberg gait Positive trendelenberg sign Poor sit to stand

Question 14

Extra signs to look for in proximal myopathy that may point to cause?

Answer 14

Heliotrope rash and gottrons papules in dermatomyositis Surgical scars (ie in chest) for paraneoplastic syndrome

Question 15

What are the causes of proximal myopathy - the most likely differential for proximal muscle weakness?

Answer 15

Congenital: Muscular dystrophy - Duchenne’s, Beckers, Emery Dreyfuss, Limb girdle, Fascioscapulohumeral dystrophy Metabolic myopathies - glycogen and lipid storage disorders Acquired: Inflammatory myositis - polymyositis, dermatomyositis, inclusion body myositis Paraneoplastic Infection - HIV, infectious pyomyositis, trichinosis, cysticerosis, coxsackie virus, lyme disease. Endocrine - thyroid disease, Cushings, acromegaly, hypopituitarism, Metabolic - periodic paralysis Toxins - alcohol, steroids, statins, cocaine. Sarcoidosis

Question 16

Causes of distal muscle weakness?

Answer 16

Tend to be neurological in cause rather than a muscle problem. Unilateral - Radiculopathy (C8-T1), Bracial plexopathy, peripheral nerve lesion. Bilateral: Guillian barre syndrome Chronic inflammatory demyelinating polyneuropathy Multifocal motor neuropathy with conduction block Motor neurone disease Inclusion body myositis (hands and forearms) Myotonic dystrophy Congenital distal myopathies

Question 17

How does distal weakness present on exam?

Answer 17

wasting of the small muscles of the hand Foot drop Distal reduction in power Distal functional impairment - difficulty opening jars, turning a key, buttoning a shirt.

Question 18

What would you expect to find in exam for multiple sclerosis?

Answer 18

Optic neuritis Internuclear ophthalmoplegia Lhermitte’s sign Upper motor neurone weakness Dorsal column (vibration/proprioception) sensory loss Cerebellar involvement - ataxia, dysarthria, dysmetria, dydiadochokinesis, nystagmus

Question 19

What are the signs of optic neuritis (seen in MS?)

Answer 19

Reduced visual acuity, central visual loss, reduced colour perception, optic disc atrophy.

Question 20

What is internuclear ophthalmoplegia (seen in MS?)

Answer 20

Inability to adduct one eye, with nystagmus in the other eye.

Question 21

What is lhermitte’s sign?

Answer 21

Seen in MS - electric sensation down the spine and in the limbs on neck flexion

Question 22

What is chronic inflammatory demyelinating polyneuropathy?

Answer 22

Like the chronic form of Guillain Barre, need symptoms for at least 8 weeks, presumed autoimmune but antibody not identified, responds somewhat to prednisone, IVIG and plasmapheresis but not really reversible. EMG and nerve conduction consistent with demyelinating neuropathy.

Question 23

What examination findings would you expect in CIDP?

Answer 23

Symmetrical lower motor neurone weakness Distal > proximal (foot drop) Upper limb > lower limb Glove and stocking distribution of sensory loss

Question 24

What is myasthenia gravis?

Answer 24

Autoimmune condition with antibodies against the acetyl choline receptor. Causes fatiguability of muscles - particularly involving eye movement, eye lid opening and shoulder abduction. Improves with the cold (ice test). Treated with pyridostigmine. Often associated with a thymoma.

Question 25

What examination findings would you expect in myasthenia gravis?

Answer 25

Skeletal muscle fatiguability: Simpson’s test - ptosis on sustained upward gaze. Proximal muscle fatiguability - compare shoulder abduction power - exercise one side with 20 chicken wing movements - then compare power with other side. Bulbar fatiguability - development of nasal speech as paragraph is read Thymectomy scar in neck

Question 26

What are some bedside tests, blood tests and imaging that you could order in myasthenia gravis?

Answer 26

Bedside - ice test Blood test - acetyl choline receptor antibodies, other antibodies (LEMs etc) Imaging - CT chest looking for thymoma

Question 27

What are the Neurological examination findings in myotonic dystrophy?

Answer 27

Myopathic facies - temporalis wasting, mandibular wasting, frontal baldness Flaccid dysarthria - nasal speech, breathiness, monotony, impaired articulation. Warm up phenomenon - grip myotonia, repeated eye closure Percussion myotonia - Muscle contraction with percussion of thenar eminence. Wasting of the small muscles of the hand and forearm. Distal muscle weakness Hyporeflexia

Question 28

What are all the ways in which myotonic dystrophy affects the body?

Answer 28

Myotonia Cognitive impairment Cataracts Hearing impairment Endocrine - diabetes, hypogonadism, secondary hyperparathyroidism Cardiovascular - arrhythmia, cardiomyopathy, sudden cardiac death Respiratory - obstructive sleep apnoea Gastrointestinal - transaminase elevation, constipation/diarrhoea. Hypogammaglobulinemia

Question 29

What is myotonic dystrophy?

Answer 29

Most common form of muscular dsytrophy, classically presenting in 30s, characterised by progressive muscle weakness and myotonia (ie, abnormally slow or delayed muscle relaxation following a normal muscle contraction). Lots of associated abnormalities (cardiac, diabetes, infertility). Main types are DM1 and DM2. Autosomal dominant.

Question 30

How are the 2 main types of myotonic dystrophy (DM1 and DM2) different?

Answer 30

DM1 more severe than DM2. Life expectancy reduced in DM1 but not DM2. Different pattern of weakness - DM1 affects facial muscle, bulbar muscles and distal muscles primarily whereas DM2 affects proximal muscle (hip girdle) mainly. Clinical myotonia is less common in DM2 but present in most cases of DM1

Question 31

What is the diagnostic test for myotonic dystrophy?

Answer 31

Genetic testing for an expanded CTG repeat in the DMPK gene is the gold standard for confirming the diagnosis of DM1. Electromyography (EMG) will usually demonstrate the presence of myotonia if this has not been found clinically or if uncertainty persists regarding its presence or absence on examination

Question 32

What would be included in the work up for myotonic dystrophy once diagnosis confirmed?

Answer 32

Depending to some degree upon the phenotype, most patients with DM1 and DM2 may need cardiac evaluations for arrhythmia and cardiomyopathy; forced vital capacity (FVC) for respiratory muscle weakness; polysomnography for sleep disorders; ophthalmologic examination for cataracts; swallowing assessment for dysphagia; cognitive and psychosocial assessments for intellectual, attentional, and psychiatric disorders; and endocrine testing for diabetes and hypothyroidism.

Question 33

Are there any medications you can give for myotonic dystrophy?

Answer 33

Not to change prognosis - however: or occasional adult patients who have severe myotonia that interferes with function, we suggest initial therapy with mexiletine 450 or 600 mg daily in three divided doses. For adult patients with DM1 and severe (excessive daytime sleepiness) EDS, we suggest a trial of modafinil (200 mg twice daily

Question 34

What is mmn with cb?

Answer 34

Multifocal motor neuropathy with conduction block. Very rare disease. autoimmune attack on peripheral motor nerves. antibodies to GM1 and evidence of demyelination with conduction block in peripheral motor nerves. Distal to proximal. Asymmetric in nature (as opposed to GBS or CIPD). No sensory involvement! Some response to IVIG (pred and plasma exchange worsen). Presents with difficulty using hands, keys, dropping things.

Question 35

What is charcot marie tooth disease

Answer 35

refers to multiple genetic conditions causing demyelination or axonal damage of peripheral nerves. some forms x linked. Weakness, wasting of muscles in hands and feet. Pes cavus (high arch), hammer toes. sensory involvement- progressive, no cure. physio, pain relief. most patients remain ambulatory.

Question 36

What is charcot marie tooth disease

Answer 36

refers to multiple genetic conditions causing demyelination or axonal damage of peripheral nerves. some forms x linked. Weakness, wasting of muscles in hands and feet. Pes cavus (high arch), hammer toes. sensory involvement- progressive, no cure. physio, pain relief. most patients remain ambulatory.

Question 37

What are the features of motor neurone disease on examination?

Answer 37

Can be upper motor neurone, lower motor neurone or both. But only affects motor nerves - no sensory involvement. As can be either upper or lower motor neurone, can therefore get bulbar and/or pseudo bulbar palsy.

Question 38

What is the difference between bulbar and pseudo bulbar palsy?

Answer 38

Bulbar palsy (LMN - think B for bottom) - nasal speech (as cant exclude air from nasal cavity when talking due to muscle palsy), absent gag reflex, tongue wasting and fasiculations, absent palate rise, absent (ie normal) jaw jerk. Pseudobulbar palsy (UMN) - dysarthria, increased/normal gag reflex, tongue spasticity, absent palate rise, increased jaw jerk.

Question 39

What is NOT involved in motor neurone disease?

Answer 39

No sensory involvement or ocular palsies

Question 40

What are the features of amyotrophic lateral sclerosis?

Answer 40

Type of motor neurone disease in which there is mixed upper and lower motor neurone involvement.

Question 41

What are the features of primary lateral sclerosis?

Answer 41

Type of motor neurone disease in which there is mainly upper motor neurone involvement. Loss of upper motor neurons results in slowness of movement, incoordination, and stiffness with relatively little overt weakness. Arm or hand upper motor neuron symptoms include poor dexterity with resulting difficulty performing activities of daily living. Leg upper motor neuron symptoms manifest as a spastic gait with poor balance and may include spontaneous leg flexor spasms and ankle clonus

Question 42

What are the features of progressive muscular atrophy?

Answer 42

Type of motor neurone disease in which the is mainly lower motor neurone involvement. Loss of lower motor neurones results in weakness, usually accompanied by atrophy and fasciculations. Muscle cramps are also common. Hand weakness causes difficulty manipulating small objects (buttons, zippers, coins) and using writing instruments. Proximal arm weakness results in difficulty elevating the arm to the level of the mouth or above the head. This can produce difficulty with bathing, dressing, grooming, and eating. Foot and ankle weakness results in tripping, a slapping gait, and falling. Proximal leg weakness results in difficulty arising from chairs, climbing stairs, and getting off of the floor. Balance may also be adversely affected. Lower motor neurone weakness affecting the trunk and spine may produce difficulty holding up the head and difficulty maintaining an erect posture as well as abdominal protuberance

Question 43

What are the features of progressive bulbar palsy?

Answer 43

Type of motor neurone disease in which there is mainly bulbar involvement. Dysarthria and dysphagia are the most common bulbar upper motor neuron symptoms (table 2). Upper motor neuron or spastic dysarthria produces a characteristically strained vocal quality with slow speech. Upper motor neuron dysphagia results from slow and discoordinated contraction of the swallowing muscles, which may lead to coughing and choking. Another frequent bulbar upper motor neuron symptom is the syndrome of the pseudobulbar affect [36,37]. This is manifested as inappropriate laughing, crying, or yawning. This may occur as an early manifestation of ALS or may develop during the disease course

Question 44

What is motor neurone disease?

Answer 44

Progressive neurodegenerative disorder affecting motor neurones leading to muscle weakness and eventually death. Usually sporadic rather than familial (10% only). ALS is the most common form.

Question 45

What are the features of flail arm and flail leg syndrome?

Answer 45

Variants of motor neurone disease where there is asymmetrical lower motor neurone involvement of a single limb - weakness of proximal arm or leg that slowly progresses distally. Better prognosis, slower progression than other types of motor neurone disease.

Question 46

How does ALS (most common form of motor neurone disease) typically present.

Answer 46

Weakness starting in asymmetrical nature in hand or foot, proximal start less common. Can be upper or lower motor neurone. Look for foot drop and split hand syndrome.

Question 47

What is split hand syndrome?

Answer 47

Wasting of the hand in ALS in a way that affects the thenar muscles more than the hypothenar. Quite specific for ALS.

Question 48

What are the patterns of weakness in the different types of myositis?

Answer 48

Polymyositis and dermatomyositis usually present with proximal weakness including neck extensor weakness. Inclusion body myopathy often presents with weakness in the quadriceps and weakness in the finger flexors that is out of proportion to intrinsic hand muscle weakness.

Question 49

What signs point to cerebellar pathology on examination?

Answer 49

Wide based, ataxic gait Dysarthria Intention tremor Dysmetria - can’t judge distance - over or undershoot Disdiadochokinesis Muscle wasting Nystagmus

Question 50

What is a list of differentials for cerebellar pathology?

Answer 50

Trauma Vascular - ischemia, haemorrhage Malignancy Demyelination Drugs and toxins such as alcohol, lithium, phenytoin, chemo. Inherited causes - friedreich ataxia, spinocerebellar ataxia Paraneoplastic Hypothyroidism

Question 51

What is friedreich ataxia?

Answer 51

Friedreich ataxia, a neurodegenerative disorder that is the most common of the hereditary ataxias, autosomal recessive. Result of mitochondrial accumulation of iron, which may promote injury caused by oxidative stress due to genetic defect (loss of function mutations in the frataxin (FXN) gene). The major clinical manifestations of Friedreich ataxia are neurologic dysfunction, cardiomyopathy, and diabetes mellitus. Reduced life expectancy, usually due to heart problems.

Question 52

What is spinocerebellar ataxia?

Answer 52

Term used to describe the autosomal dominant inherited ataxias of which there are many. Do genetic testing then MRI if unrevealing .

Question 53

What are the neurological features of friedreich’s ataxia?

Answer 53

Progressive ataxia of limbs and gait Loss of reflexes (later). Motor weakness - lower limbs first then upper. Can get pes cavus and hammer toes. Cerebellar dysarthria Sensory loss in the distal limbs (proprioception and vibration sense) - pain and temp preserved. Dysphagia Reduced visual acuity, eye movement problems. Hearing loss eventually Bladder dysfunction (urgency - incontinence.) OSA

Question 54

Differentials for bulbar palsy?

Answer 54

Due to cranial nerve dysfunction (9, 10, 12) Motor neurone disease Guillian Barre syndrome Polio Neurosyphillus Brainstem stroke

Question 55

Differentials for pseudo bulbar palsy?

Answer 55

Upper motor neurone pathology of CN 9,10,12 Internal capsule stroke Multiple sclerosis Motor neurone disease Head injury

Question 56

What are the findings in cerebellopontine angle syndrome?

Answer 56

Trigeminal (V) nerve palsy - reduced facial sensation Facial (VII) nerve palsy - facial droop / weakness Vestibulocochlear (VIII) nerve palsy - unilateral sensorineural hearing loss, (bruns) nystagmus, ataxia

Question 57

What are the differentials for cerebellopontine angle sydrome?

Answer 57

caused by a malignancy affecting the cerebellopontine angle: Vestibular schwannoma Meningioma Cerebellar astrocytoma Brain metastasis

Question 58

What will a complete transection of the spinal cord cause?

Answer 58

Segmental syndrome - sensory loss and upper motor neurone weakness below the affected level with bladder and bowel dysfunction.

Question 59

What are the findings in a central cord syndrome - usually caused by C spine trauma or hyperextension of the cervical spine?

Answer 59

Bilateral upper motor neurone weakness affecting the upper limbs more than the lower limbs and loss of proprioception and vibration.

Question 60

Proprioception and vibration are carried by?

Answer 60

the dorsal column (posterior aspect of cord)

Question 61

What are the findings in a ventral cord syndrome - caused by anterior compression of the spinal cord or anterior spinal artery pathology?

Answer 61

Upper motor neurone weakness and loss of pain and temperature sensation, but preservation of proprioception and vibration sensation.

Question 62

Pain and temperature are carried by?

Answer 62

the spinothalamic tract (anterio-lateral aspect of cord)

Question 63

What are the findings in posterior compression of the spinal cord, or posterior spinal artery pathology (dorsal cord syndrome?)

Answer 63

Loss of proprioception and vibration sense (dorsal column) but preservation of motor function (corticospinal tract) and preservation of spinothalamic tract (pain and temp)

Question 64

What is brown sequard syndrome and what are the examination findings?

Answer 64

Hemitransection of the spinal cord - ipsilateral upper motor neurone weakness and ipsilateral loss of proprioception and vibration (dorsal column), with contralateral loss of pain and temperature sensation (spinothalamic tract).

Question 65

What is conus medullaris syndrome and what are the examination findings?

Answer 65

Distal upper and lower motor neurone weakness with perineal loss of sensation (saddle anaesthesia), urinary retention and faecal incontinence.

Question 66

What is the difference between conus medullaris and cauda equina syndromes?

Answer 66

Conus medullaris is a squeeze at L1-L2 (the bulbous end of the spinal cord as the cauda equina comes out. Cauda equina is a squeeze lower down L2-L5 where there are only lower motor neurones. Both present with: Motor or sensory deficits in the legs – usually bilateral Lower motor neuron signs in the legs – areflexia, hypotonia Saddle anaesthesia Absent or decreased rectal tone Absent or decreased bulbocavernosus reflex Palpable bladder indicating urinary retention However It is important to note that in the case of isolated conus medullaris syndrome, deficits of the lower extremities are more often bilateral and symmetric. Also, upper motor neuron signs can be present, such as spasticity and hyperreflexia

Question 67

L2, L3, L4 radiculopathy?

Answer 67

L2, L3, and L4 radiculopathies are most often seen in older patients with spinal stenosis. They are generally considered as a group because of marked overlap of innervation of the anterior thigh muscles. Acute back pain is the most common presenting complaint, often radiating around the anterior aspect of the thigh down into the knee.

Question 68

L5 radiculopathy?

Answer 68

L5 radiculopathy is the most common radiculopathy affecting the lumbosacral spine. It often presents with back pain that radiates down the lateral aspect of the leg into the foot. On examination, strength can be reduced in foot dorsiflexion, toe extension, foot inversion, and foot eversion. Reflexes are generally normal.

Question 69

L5 radiculopathy?

Answer 69

L5 radiculopathy is the most common radiculopathy affecting the lumbosacral spine. It often presents with back pain that radiates down the lateral aspect of the leg into the foot. On examination, strength can be reduced in foot dorsiflexion, toe extension, foot inversion, and foot eversion. Reflexes are generally normal.

Question 70

S1 radiculopathy?

Answer 70

In S1 radiculopathy, pain radiates down the posterior aspect of the leg into the foot from the back. On examination, strength may be reduced in leg extension (gluteus maximus) and plantar flexion. Sensation is generally reduced on the posterior aspect of the leg and the lateral foot. Ankle reflex loss is typical.

Question 71

What are the differentials for lumbrosacral radiculopathy?

Answer 71

In addition to a herniated disc, the differential diagnosis of lumbosacral radiculopathy includes lumbar spinal stenosis, cauda equina syndrome, diabetic amyotrophy, lumbosacral plexopathy, and mononeuropathies of the leg, such as femoral, sciatic, peroneal, and tibial nerve lesions.

Question 72

Common peroneal nerve pathology

Answer 72

Damaged at the fibular neck, just below the knee. Usually caused by prolonged lying, leg crossing, squatting, leg cast or fracture of fibular neck. Symptoms: Foot drop, paresthesias and/or sensory loss over dorsum of foot and lateral shin. Signs: Weakness on foot dorsiflexion and eversion; sensory loss on dorsum of foot; reflexes normal. (Remember pEroneal = weak Eversion of ankle, Lfive = weak Inversion of ankle)

Question 73

Common peroneal nerve pathology?

Answer 73

Damaged at the fibular neck, just below the knee. Usually caused by prolonged lying, leg crossing, squatting, leg cast or fracture of fibular neck. Symptoms: Foot drop, paresthesias and/or sensory loss over dorsum of foot and lateral shin. Signs: Weakness on foot dorsiflexion and eversion; sensory loss on dorsum of foot; reflexes normal. (Remember pEroneal = weak Eversion of ankle, Lfive = weak Inversion of ankle)

Question 74

Deep peroneal nerve pathology?

Answer 74

Usually injured at the ankle by a tight fitting shoe or strap. Symptoms: Ankle pain, foot drop and sensory loss over web space between digits 1 and 2.

Question 75

Posterior tibial nerve pathology?

Answer 75

Usually damaged in the tarsal tunnel of the ankle by fracture or dislocation of talus, calcaneus, medial malleolus, rheumatoid arthritis or a tumor. Symptoms: Aching, burning, numbness, tingling on sole of foot, distal foot, toes, and occasionally heel. Signs: Positive Tinel’s sign over nerve posterior to medial malleolus; sensory loss on sole of foot; atrophy of foot muscles if severe

Question 76

Sciatic nerve pathology?

Answer 76

If damaged at the sciatic notch (gluteal region) - most commonly by trauma (hip dislocation, fracture, or replacement), prolonged bed rest, deep-seated pelvic mass, piriformis syndrome there will be leg pain and weakness affecting most lower leg muscles. If damaged mid thigh by a femur fracture, mass, ischemic nerve infarction the weakness will spare the hamstrings. Signs: Sensory loss in peroneal, tibial, and sural territories; may spare medial calf and arch of foot; normal knee jerk; absent ankle jerk

Question 77

Femoral nerve pathology?

Answer 77

Normally damaged in the pelvis or anterior thigh by hip or pelvic fracture, hip replacement, lithotomy position, diabetes mellitus. Symptoms: Quadriceps weakness and sensory loss over anterior thigh. Signs: Quadriceps weakness; sensory loss over anterior and medial thigh extending down medial shin to arch of foot; reduced or unobtainable knee jerk.

Question 78

Lateral cutaneous nerve of thigh pathology?

Answer 78

Normally damaged at the inguinal ligament (meralgia paresthetica) by obesity, tight fitting belts, idiopathic, pregnancy. Symptoms: Paresthesias and pain radiating down the lateral thigh to knee. Signs: Sensory loss on lateral thigh.

Question 79

Pathology of obturator nerve?

Answer 79

Rare, potentially caused by pelvic tumor such as TCC of the bladder resulting in compression. Results in pain, weakness in leg adduction, and sensory loss over a small area in the medial thigh.

Question 80

unilateral foot drop with ankle jerk preserved, ankle inversion power preserved and sensation loss over lateral foot and leg?

Answer 80

Common peroneal nerve injury at knee

Question 81

unilateral foot drop with ankle jerk preserved, ankle inversion power preserved and sensation loss between 1st and 2nd toe?

Answer 81

Deep peroneal branch of common peroneal nerve as it passes through ankle.

Question 82

Unilateral foot drop with loss of ankle jerk and complete loss of sensation and power below the knee?

Answer 82

Sciatic nerve lesion

Question 83

Unilateral foot drop with loss of ankle jerk and loss of sensation in dermatomal distribution?

Answer 83

Cauda equina syndrome

Question 84

Bilateral foot drop with normal reflexes?

Answer 84

Distal neuropathy (LMN), myopathy

Question 85

Bilateral foot drop with increased reflexes?

Answer 85

Conus medullaris or other spinal cord pathology Upper motor neurone lesion

Question 86

unilateral foot drop with ankle jerk preserved, ankle inversion power reduced and additional weakness of hip abduction and knee flexion.

Answer 86

L5 nerve root lesion

Question 87

In an ataxic gait due to a cerebellar lesion the person will fall towards or away from the side of the lesion?

Answer 87

Will fall towards the side of the lesion

Question 88

What are the examination findings in fascioscapulohumeral dystrophy?

Answer 88

Facial weakness - particularly obicularis occuli Winging of the scapular preventing full shoulder abduction - may have scar from scapular fixation to increase ROM Bicep and tricep atrophy Foot drop High frequency hearing loss Retinal telangectasia

Question 89

What is fascioscapulohumeral dystrophy?

Answer 89

Facioscapulohumeral muscular dystrophy (FSHD) is the third most common type of muscular dystrophy. It is a complex genetic disorder characterised in most cases by slowly progressive muscle weakness involving the facial, scapular, upper arm, lower leg, and hip girdle muscles, usually with asymmetric involvement. Caused by inappropriate expression of the DUX4 gene. Other manifestations of FSHD may include pain, retinal vasculopathy, hearing loss, cardiac arrhythmia, cognitive impairment, and epilepsy. The management of FSHD is primarily supportive, as no disease-modifying therapy is available.

Question 90

what are the findings in an isolated 4th nerve (trochlear) palsy?

Answer 90

when eye on affected side tries to move towards the nose it drifts upwards due to paralysis of superior oblique muscle which is responsible for pulling eye down and torsional movements. patients get double vision as a result and end up walking with head tilted away from affected side to compensate. difficulty walking down stairs and reading a book many causes of trochlear nerve palsy as long and tortuous nerve.

Question 91

What are the findings in an isolated 3rd nerve (occulomotor) palsy?

Answer 91

pupil down and out on affected side, ptosis, possibly pupil dilated. if surgical cause, ie external compression, then pupil will be dilated. important example includes posterior inferior communicating artery aneurysm. if medical cause, ie nerve problem from inside out then pupil constriction will be conserved until very severe.

Question 92

what are the findings in an isolated 6th nerve (abducens) palsy?

Answer 92

double vision in horizontal gaze to side of lesion. lateral rectus muscle palsy. unable to abduct affected eye causes include stroke but also a finding in benign intercranial hypertension (in which there would also papillo oedema on fundoscopy)

Question 93

Pattern 1: Symmetric proximal and distal weakness with sensory loss

Answer 93

Consider: inflammatory demyelinating polyneuropathy (GBS and CIDP)

Question 94

Pattern 2: Symmetric distal sensory loss with or without distal weakness

Answer 94

Consider: cryptogenic sensory polyneuropathy (CSPN) metabolic disorders drugs, toxins hereditary (Charcot-Marie-Tooth, amyloidosis and others)

Question 95

Pattern 3: Asymmetric distal weakness with sensory loss

Answer 95

Multiple nerves, consider: vasculitis hereditary neuropathy with liability to pressure palsies (HNPP) multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy infectious (leprosy, lyme, sarcoid, HIV) Single nerves/regions, consider: compressive mononeuropathy and radiculopathy

Question 96

Pattern 4: Asymmetric proximal and distal weakness with sensory loss

Answer 96

Consider: polyradiculopathy or plexopathy due to diabetes mellitus, meningeal carcinomatosis or lymphomatosis, sarcoidosis, amyloidosis, Lyme, idiopathic, hereditary (HNPP, familial)