Week 12 Neuro Part 2

Question 1

Restless leg syndrome - what is it? When does it occur?

Answer 1

-common sensorimotor disorder associated with unpleasant sensations (prickling, tingling, crawling) and undesired periodic leg movements

-occur at rest and worse in the evening or at night

-powerful urge to move legs for relief-can significantly affect sleep/QOL

Question 2

Are periodic limb movements always a part of restless leg syndrome?

Answer 2

No, can just be uncomfortable sensations that make you want to move your legs… periodic limb movements during sleep is considered its own disorder

Question 3

What populations experience restless leg syndrome more commonly?

Answer 3

more common in women, during pregnancy, older persons and individuals who are iron deficient

Question 4

When are the uncomfortable sensations of restless leg syndrome worse? (2)

Answer 4

• During rest/inactivity
• At night

Question 5

How common is it for those with restless leg syndrome to also have periodic movements of sleep (PLMS)?

Answer 5

Approximately 85% of patients with RLS have periodic movements of sleep, usually involving the legs (periodic leg movements of sleep [PLMS]). PLMS is characterized by involuntary, forceful dorsiflexion of the foot lasting 0.5-5 seconds and occurring every 20-40 seconds throughout sleep.

Question 6

Are sleep disturbances, daytime fatigue, and involuntary jerking movements (either while asleep or awake) part of the diagnostic criteria for RLS?

Answer 6

No, but they are features commonly associated with restless leg syndrome

Question 7

What do you need to test for in all patients with RLS?

Answer 7

Iron deficiency

Question 8

Do we routinely do sleep studies for people with RLS?

Answer 8

NO, but Polysomnography may be necessary to quantify PLMS or to characterize sleep architecture, especially in children and in patients who continue to have significant sleep disturbances despite relief of RLS symptoms with treatment

**Sleep disturbances may be associated with RLS but are not part of the diagnostic crtieria

Question 9

What are some non-pharmacologic treatments of RLS?

Answer 9

Sleep hygiene measures

Avoidance of caffeine, alcohol, and nicotine in patients with mild RLS who are sensitive to these substances

Discontinuation, when possible, of medications that cause or exacerbate RLS, such as selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinepherine reuptake inhibitors (SNRIs), diphenhydramine, and dopamine antagonists

Exercise

Physical modalities before bedtime, such as a hot or cold bath, whirlpool bath, limb massage, and vibratory or electrical stimulation of the feet and toes

Question 10

What is Periodic Limb Movements Disorder? (PLMD)

Answer 10

Is sleep disorder

Often co-exists with restless leg syndrome, but is a distinct and mutually exclusive diagnosis

Movements occur AFTER You fall asleep (RLS is more about what leg discomfort BEFORE sleep)

characterized by a clinical sleep disturbance attributed to an increased number of PLMS (periodic limb movements of sleep), in the absence of alternative causes of the sleep complaints.

Question 11

Cause of PLMS?

Answer 11

Causes largely not understood, but seems to be associated with many of same conditions as RLS: low ferritin levels, medications,

According to Wikipedia…PLMS seems to have an origin in the spinal cord. In fact, PLMS was suggested to be associated with increased spinal reflexes. Manifestations of PLMS seem to occur mostly in disorders associated with dopaminergic dysfunctions

Question 12

Do periodic limb movements of sleep occur during REM or NREM sleep?

Answer 12

Occurs during non-REM sleep stages (do not occur during REM due to muscle atonia)

Question 13

S&S of periodic limb movement disorder?

Answer 13

Usually manifests as daytime somnolence

Wake up with cramps or “Charlie horse” In legs

Often not aware of these movements at all, unless someone else points them out (bed partner may complain of person kicking them during sleep)

During night, leg twitching or jerking (usually flexion) movements during sleep occurring every 15 to 40 seconds.

Question 14

Do you need to do a sleep study to diagnose perioid limb movement disorder? What is included in the diagnostic criteria?

Answer 14

Yes! (unlike RLS)
diagnosed based on a clinical history of sleep disturbance or daytime fatigue, combined with polysomnography (PSG) showing an excessive number of periodic limb movements of sleep (PLMS), and exclusion of alternative causes of the sleep complaints.

Diagnostic criteria = more than 15 periodic limb movements per hour of sleep time in adults (more than 5 in children), causing clinically significant sleep disturbance or impairment in function or wellbeing not explained by some other entity

PLMD is a diagnosis of exclusion and cannot be diagnosed in the context of other sleep disorders that have already been diagnosed, such as RLS, OSA, and narcolepsy (because these present with very similar movements)

Question 15

What areas of muscle does the ulnar nerve innvervate?

Answer 15

some forearm and most hand muscles

• Flexor carpi ulnaris muscle
• The ulnar half of the flexor digitorum profundus muscle in the anterior forearm
• Most of the intrinsic hand muscles: hypothenar muscles, two lumbricals, adductor pollicis muscle, all the interossei muscles (palmar and dorsal)

Question 16

What is happening when you feel like you “hit your funny bone”?

Answer 16

The ulnar nerve is vulnerable as it passes posterior to the medial epicondyle of the humerus

This causes the “I hit my funny bone” tingling sensation

Question 17

What spinal nerves does the ulnar nerve originate from?

Answer 17

From the brachial plexus: spinal nerves C7, C8 and T1

The ulnar nerve is a terminal branch of the medial cord of the brachial plexus. It contains mainly fibers from the anterior rami of spinal nerves C8 and T1, but may sometimes carry C7 fibers as well.

Question 18

Is the ulnar nerve motor or sensory or both?
Why is it considered one of the most clinically relevant nerves of the upper limb?

Answer 18

From its origin, the ulnar nerve courses distally through the axilla, arm and forearm into the hand. It is a mixed nerve and provides motor innervation to various muscles of the forearm and hand as well as sensory supply to the skin of the hand.

The ulnar nerve can broadly be described as the nerve of the hand, as it innervates the vast majority of the intrinsic hand muscles. It is one of the most clinically relevant nerves of the upper limb, due to its superficial course and clinically apparent role in hand function.

Question 19

S&S of diabetes-associated peripheral neuropathy?

Answer 19

Distal symmetrical sensorimotor polyneuropathy with glove and stocking loss of sensations such as: pain, vibration, temperature, proprioception.

Loss of motor function with clawed toes and small muscle wasting in hands and flexor muscles

Charcot joints: loss of sensation results in joint and ligament degeneration, particularly of the foot

Numbness

Loss of balance

Tingling

Pain

Question 20

Clinical tests to screen for diabetes associated peripheral neuropathy

Answer 20

Careful history

Assessment of small nerve fibre function by testing thermal or pin prick sensation and light touch perception with a 10 g monofilament on the dorsal aspect of the distal great toe

Assessment of large nerve fibre function by testing vibration sensation with a 128 Hz tuning fork, proprioception (joint position sensation), and deep tendon reflexes at the ankle as compared with more proximal locations

Ankle and patellar deep tendon reflexes

Extension of the big toe, ankle dorsiflexion, and walking on heels to test motor strength

Romberg test, normal gait, and tandem gait to assess balance and fall risk. Pt stands with feet together (a soldier at attention) then they close their eyes.

Clinical assessment of the lower legs and feet to look for any ulceration or deformity

Question 21

Causes of upper motor neuron lesions? What areas would the lesions be in to cause upper motor neuron issues?

Answer 21

Any injury to brain (stroke, infection, tumors), brainstem, or white matter of spinal cord.

Question 22

What is a lower motor neuron lesion? Where is it occuring?

Answer 22

• Any damage to the lower motor neuron axon, which goes from the spinal cord to the muscle.
• Any injury to the ventral grey matter of the spinal cord (because this is where the lower motor neuron starts)

Question 23

What effect does an upper motor neuron lesion have on deep tendon reflexes? Superficial reflexes?

Answer 23

Deep tendon are HYPERFLEXIC –> reflex becomes amplified because upper motor neurons are not able to regulate reflex at that level.

Superficial reflexes - diminished or absent
(Babinski reflex is positive)

Question 24

Do you see muscle atrophy more in upper or lower motor neuron lesions?

Answer 24

Lower, because lower is what would normally deliver impulse to muscles directly. (may see weakness but not so much atrophy in upper motor neuron lesions)

Question 25

Would you see a plantar response (babinski) if lower motor neuros lesions?

Answer 25

No

Question 26

What is the effect of lower motor neuron lesions on deep tendon reflexes?

Answer 26

Absent

Question 27

Would you see fasciculations in muscles with upper or lower motor neuron lesions?

Answer 27

Lower.... in this case, muscle may be affected but are still some single muscle fibres that are still stimulated (still some transmission from lower motor neurons that are not injured)

Question 28

How common is huntington's disease? How likely are you to inherit it if parents have it?

Answer 28

~ 1 in 7000 people affected in Canada Hereditary If one parent has HD 50 % chance, it’s passed on --> Is autosomal DOMINANT trait

Question 29

Patho of huntington's disease (HD). What chromosome is affected?

Answer 29

HD defect is on chromosome 4 Short version: abnormal DNA sequencing --> abnormal protein formation --> altered motor & mental functions Repeated sequence of DNA (CAG nucleotides) causes formation of abnormal Protein leading to altered motor and mental functions People with HD have 36 or more CAG (Glutamine) repeats on Huntingtin (HTT) gene (also referred to Polyglutamine disease) Normal: 10-35 times in a row Chains of glutamine stick together and contribute to neuronal loss Progression leads to tissue loss in basal ganglia Recap Basal Ganglia Function: involved in motor function by providing feedback mechanism to motor cortex for initiation & control of voluntary movements Regions affected by HD have decrease GABA and Acetylcholine and increased Dopamine levels

Question 30

When does huntington's usually present? Is it fatal? Fast or slow to progress?

Answer 30

Progressive, slow, fatal Onset is usually around 40 years of age The more repeats of CAG the earlier the onset of symptoms Neuroradiological abnormalities can occur up to 15 years before clinical symptoms

Question 31

What are the motor symptoms of huntington's disease

Answer 31

Movement inhibition Excessive involuntary movements Hypotonia with hyperreflexia (early symptom), chorea (ex. Face, head, neck, tongue, trunk, extremities), athetosis, dystonia, eye movement slows, gait abnormalities (unsteady, irregular -> bradykinesia, rigidity late in disease)

Question 32

What are the psychiatric, cognitive, and physical appearance symptoms of huntington's disease

Answer 32

Apathy, irritability, depression, delusions, aggressions, disinhibition, paranoia Cognitive: Progressive dementia, inflexibility of thought, decreased insight and concentration, memory loss Weight loss, cachexia

Question 33

How to diagnose Huntington's disease?

Answer 33

MRI shows atrophy of head of caudate nuclei Genetic testing for CAG repeats in HTT gene. Normal = 10-35 repeats. >36 repeats = HD Other: History, physical examination neurological: motor and mental status exams

Question 34

Common causes of peripheral neuropathy?

Answer 34

commonly from diabetes mellitus, alcohol abuse, HIV infection Other systemic causes of neuropathy (mostly axonal polyneuropathies) include chronic HIV infection, critical illness, end stage kidney disease, amyloidosis, hypothyroidism, vitamin deficiencies, lyme disease Autoimmune polyneuropathies (most notably Guillain-Barre syndrome) are mostly demyelinating neuropathies Toxic polyneuropathies are mostly from toxins including alcohol, chemotherapy exposure, heavy metals (causes a predominantly axonal polyneuropathy that could be acute, subacute or chronic

Question 35

How do we describe the typical distribution of onset of peripheral neuropathy? What symptom is characteristic of acute polyneuropathies?

Answer 35

Weakness of lower legs and hands start as the syndrome progresses (the classic "stocking and glove" distribution of sensory loss) Some polyneuropathies are acute (mainly caused by toxins), and those are characterized by pain

Question 36

In peripheral neuropathies, do you typically see onset of sensory symptoms or motor symptoms first? What cause is a relatively common exception to this?

Answer 36

Sensory Guillain Barre syndrome mostly affects motor neurons, and is an acute demyelinating polyneuropathy, and tends to first present with weakness instead of sensory loss

Question 37

Diagnostic testing for peripheral neuropathies?

Answer 37

Clinical exam, extensive diagnostic testing usually unnecessary if mild symptoms with a known underlying cause (ie. Diabetes, alcohol abuse or chemotherapy) Full diagnostic testing is warranted for those with no clear cause, or if symptoms are severe and rapidly progressive Electrodiagnostic testing (with electromyography- EMG- and/or nerve conduction studies are initial testing when there is no clear etiology, or symptoms are rapidly progressive or severe

Question 38

What are some s/s of Obstructive Sleep Apnea Syndrome (OSAS)?

Answer 38

Excessive loud snoring Gasping Multiple apneic episodes (temporary pause of breathing) that lasts 10 seconds or longer

Question 39

What are some related progressions/manifestations that may be seen/associated in a patient with OSAS?

Answer 39

Obesity hypoventilation syndrome: may be r/t leptin resistance (leptin is a resp stimulant). OSAS leads to hypercapnia and decreased O2 sats -> eventually leads to polycythemia, pulmonary hypertension, systemic hypertension, stroke, right-sided heart failure, dysrhythmias, liver congestion, cyanosis, and peripheral edema. Hypersomnia (excessive daytime sleepiness) – can be so severe that people may fall asleep while talking, working, driving. Impaired mood and cognitive function; symptoms include impairment of attention, episodic memory, working memory, and executive functions.

Question 40

What are some treatment options for a person with OSAS?

Answer 40

CPAP, dental devices, surgery of upper airway and jaw if indicated, and obesity management

Question 41

What is the most common complication of diabetes?

Answer 41

Peripheral neuropathy.

Question 42

True or false? Diabetic peripheral neuropathy incidence is higher in men, starts at an earlier age in men, and has a higher likelihood of causing muscle weakness in men. However, neuropathic pain is higher in women.

Answer 42

True.

Question 43

____________ ___________ leads to gradual loss of integrity of the longest nerve fibres with symptoms starting distally in the toes and feet

Answer 43

Diabetic neuropathy.

Question 44

What is happening to nerve cells when a patient is experiencing diabetic neuropathy?

Answer 44

Demyelination contributes to neural changes and delayed conduction occurs. Both somatic and peripheral nerve cells show diffuse or focal damage resulting in polyneuropathy.

Question 45

Describe sensory neuropathies.

Answer 45

Sensory Neuropathies: loss of pain, vibration, and temperature sensation usually in hands and feet first. Begins with being asymmetric however may become symmetric over time.

Question 46

Describe motor neuropathies.

Answer 46

Motor Neuropathies: affect muscle groups, mostly in feet. These are common and may precede the sensory neuropathies or co-exist with them. Contributes to deformities and unstable balance. Alters the dynamics of walking and contributes to diabetic ulcers.

Question 47

Describe autonomic neuropathies.

Answer 47

Autonomic neuropathies: delayed gastric emptying, diabetic diarrhea, altered bladder function, impotence, orthostatic hypotension, heart rate variability (both tachy and brady), sweating.

Question 48

-Primary _____________ begins after age 40, increasing incidence after age 60 -More prevalent in males -Second most common neurogenerative disorder (from Stats Canada)

Answer 48

Parkinson's Disease

Question 49

Describe the pathophysiology of primary Parkinson's Disease.

Answer 49

Primary PD: -largely unknown -Gene/environment interactions are probable cause -Degeneration of basal ganglia with dysfunctional alpha-synuclein protein and loss of dopamine producing neurons in substantia nigra and dorsal striatum -Depletion of dopamine and excess of cholinergic activity in the feedback circuit

Question 50

In primary Parkinson's Disease, individuals with tremor-predominant symptoms at diagnosis tend to have a quicker motor progression than those with balance and gait predominant symptoms. True or false?

Answer 50

False. Those with balance and gait predominant symptoms at diagnosis tend to have a quicker motor progression.

Question 51

Patients diagnosed with primary Parkinson's Disease in middle age tend to have a slower or quicker motor progression than those diagnosed later in life?

Answer 51

People who are diagnosed in middle age or earlier tend to have slower motor progression than those diagnosed later in life.

Question 52

What effect does Parkinson's Disease have on longevity?

Answer 52

Most individuals have normal or near normal life expectancy. -Disease itself is not fatal, rather the complications (falls, etc)

Question 53

What is myasthenia gravis?

Answer 53

Definition: chronic autoimmune neuromuscular disorder that affects the neuromuscular junction and is characterized by fatiguability and weakness of voluntary muscles Hallmark: muscle weakness that increases during periods of activity and improves after periods of rest. Function best in AM, increasing weakness over course of day.

Question 54

What age ranges in men and women is myasthenia gravis most commonly seen? (5.3/million people in Canada are affected)

Answer 54

Two peaks in incidence: 1. Women in 20-30’s 2. Men in 60’s-70’s Can occur at any age, but uncommon in youth.

Question 55

What are some risk factors for developing myasthenia gravis (MG)?

Answer 55

Much is unknown Frequently manifests for first time during pregnancy! Women Exposure to anaesthetic agents Often associated with thymic hyperplasia or tumors (gland remains large and abnormal in MG) Other autoimmune disorders (SLE, RA, thyroid disease)

Question 56

What are some s/s of myasthenia gravis?

Answer 56

Classic triad: 1. Ptosis 2. Diplopia 3. Dysphagia (sense of choking) Difficulty chewing Drooling Slurring speech Easily fatiguability Symptoms more pronounced with fatigue or in evening

Question 57

What might you see upon exam if a patient has myasthenia gravis?

Answer 57

Normal to increased DTR (I don't know what DTR stands for -Gayle) Normal coordination, sensory perception, and pupillary response Eye movement dysfunction: upward/lateral gaze cannot be maintained for >30 sec Ptosis with repetitive lid closure Unable to sustain arm raise Voice quality or speech change when counting to 100

Question 58

Myasthenic crisis is life threatening and poses risk of respiratory arrest. Occurs when respiratory muscles weakened to point of needing ventilator. Usually triggered by infection, fever, or adverse reaction to medication. Signs of impending MG crisis are?

Answer 58

Sudden onset inspiratory distress Difficulty swallowing Visual difficulty Tachycardia Rapid onset weakness Quadriplegia/paresis

Question 59

Myasenthia gravis is an antibody (Ab)-mediated autoimmune attack on acetylcholine receptors (AchR) at postsynaptic membrane of neuromuscular junction. What type of hypersensitivity reaction is this?

Answer 59

Type 2

Question 60

The presentation and time course of myasenthia gravis can be highly variable, this condition can be difficult to diagnose. REFER TO NEUROLOGIST. If you suspect MG, what is a highly sensitive test you can perform in clinic? What labs can you order?

Answer 60

Clinical exam: Ice pack test: apply ice to closed eyelid X 2 mins—> very sensitive test with less ptosis post ice exposure. Thought that by cooling muscle tissue, acetylcholinesterase is inhibited. Lab test: Ab titre for Ach-receptor Ab—> positive in 90% of MG patients Anti-muscle-specific receptor tyrosine kinase Ab titre

Question 61

What are the four stages of sleep?

Answer 61

N1, N2, N3 (non-rapid eye movement stages) and REM

Question 62

Describe NREM N1 sleep stage. Which types of brain waves predominate this stage? What are some unique features of this stage?

Answer 62

Lightest stage of sleep, between wakefulness and sleep. Brain produces theta waves May experience hypnagogic hallucinations – hearing or seeing things that are not there May experience hypnic jerks – feelings of falling/muscle jerks before falling asleep

Question 63

Describe NREM N2 sleep stage. Which types of brain waves predominate this stage? What are some unique features of this stage?

Answer 63

Slightly deeper stage than N1, harder to wake More theta waves, sleep spindles and K complexes K complexes suppress cortical arousal to help keep you asleep and assist with memory consolidation

Question 64

Describe NREM N3 sleep stage. Which types of brain waves predominate this stage? What are some unique features of this stage?

Answer 64

Very deep sleep, difficult to wake Slow wave sleep, shows Delta waves The stage during which sleep walking or talking will happen

Question 65

Describe REM sleep stage. What are some unique features of this stage?

Answer 65

Also known as paradoxical sleep – because the brain is active but most muscles are paralyzed Most dreaming occurs during this stage Eyes move rapidly beneath eyelids, muscle relaxation, loss of temperature regulation, altered heart rate, BP and respirations, penile erection and clitoral enlargement

Question 66

What is the most diagnosed sleep disorder?

Answer 66

Obstructive Sleep Apnea (OSA)

Question 67

What are major risk factors for sleep apnea?

Answer 67

Obesity Male gender Older age

Question 68

Outline the pathophysiology of OSA

Answer 68

Develops when there is a blockage of the upper airways Allergies- cause swelling in the tissues of the nasopharynx Swollen adenoids/tonsils – due to infection Overbite – pulls jaw back and blocks the airway Overweight/obesity – too much weight in the soft tissues of the neck which can weigh down the airway, especially when lying down. The above are made worse by hormonal changes at night – causes the muscles around the airway to become slightly less stiff while sleeping, less able to keep the airway open and can become obstructed.

Question 69

Differentiate central sleep apnea from OSA

Answer 69

Refers to the fact that the problem stems from the CNS Brain intermittently stops making an effort to breathe for 10-30 seconds

Question 70

The characteristic “hand of benediction” or “bishop’s hand” is the presentation of which arm nerve injury?

Answer 70

Median nerve injury can result in this position by causing an inability to flex the middle and index fingers

Question 71

Describe the origin and function of the median nerve

Answer 71

Arises from the lateral and medial cords of the brachial plexus, enters the arm at the axilla and travels with the brachial artery down the humerus, into the cubital fossa and through the carpal tunnel into the hand. Innervates muscles of the anterior forearm and hand

Question 72

What percentage of ALS patients have familial ALS?

Answer 72

What percentage of ALS patients have familial ALS?

Question 73

What is the pathophysiology of ALS?

Answer 73

Motor neurons gradually breakdown and die, brain can no longer communicate with the muscles of the body, so the muscles weaken until they can no longer move

Question 74

What is the average age of onset of ALS?

Answer 74

60-75 years

Question 75

How long on average do people survive after an ALS diagnosis? What is usually the cause of death?

Answer 75

3-5 years, respiratory failure is commonly the cause of death for people with ALS

Question 76

Describe some of the signs and symptoms associated with Huntington’s disease

Answer 76

Motor symptoms: Movement inhibition, Excessive involuntary movements, Hypotonia with hyperreflexia (early symptom), chorea (ex. Face, head, neck, tongue, trunk, extremities), athetosis, dystonia, eye movement slows, gait abnormalities (unsteady, irregular -> bradykinesia, rigidity late in disease) Psychiatric : Apathy, irritability, depression, delusions, aggressions, disinhibition, paranoia Cognitive: Progressive dementia, inflexibility of thought, decreased insight and concentration, memory loss Weight loss, cachexia

Question 77

What type of exams/tests are involved in a diagnosis of Huntington’s disease?

Answer 77

MRI shows atrophy of head of caudate nuclei Genetic testing for CAG repeats in HTT gene. Normal = 10-35 repeats. >36 repeats = HD Other: History, physical examination neurological: motor and mental status exams

Question 78

Define insomnia

Answer 78

Inability to fall asleep or stay asleep Most common sleep disorder

Question 79

What are the diagnostic criteria for chronic insomnia?

Answer 79

Difficulty initiating or maintaining sleep despite adequate opportunity for sleep, with associated distress or impairment of daytime functioning lasting 3 months or longer for at least three nights each week

Question 80

What are parasomnias

Answer 80

* Unusual behaviours occurring during NRESM sleep * Sleepwalking, night terrors, rearranging furniture, exhibiting sleep sex or violent behaviour, restless leg syndrome * Somnambulism and night terrors are common in children and may be related to CNS immaturity

Question 81

Define and describe somnambulism

Answer 81

Sleep walking * Primarily a disorder of childhood and will resolve within a few years * Not associated with dreaming * Child has no memory when they wake up * When occurs in adults, commonly associated with sleep disordered breathing

Question 82

Define and describe night terrors

Answer 82

Night terrors: sudden episodes of apparent arousal with expression of strong fear or emotion * Most often occurs in children * Child is not aware, and can be difficult to arouse * When awake, child has no memory of event * Not associated with dreams * Adults also may experience with related daytime anxiety.

Question 83

Describe the path of the radial nerve through the arm

Answer 83

-BACK OF ARM: Starts at the brachial plexus (C5, C6, C7, C8, T1). Runs from radial groove to radial side of elbow to posterior forearm (runs down middle) to posterior wrist to posterior thumb, digit 1 &2

Question 84

What does the radial nerve innervate

Answer 84

Motor: Primarily extensors. Muscles that extend the forearm at the elbow (posterior compartment muscles, including the triceps brachii), extensors for the wrist, fingers, thumb. Sensory: Posterior forearm, radial side of dorsum of hand.

Question 85

Where is the radial nerve vulnerable to injury?

Answer 85

-Humeral midshaft fractures, shoulder dislocations, or arm compression injuries (trauma, tourniquets) -Can be injured by improperly fitting crutches -Also vulnerable to injury where it passes through the supinator muscle (repetitive forearm rotation; fracture) -Can also be injured near wrist (i.e., tight handcuffs)

Question 86

What nerve does carpal tunnel affect

Answer 86

Medial nerve

Question 87

Patho of carpal tunnel

Answer 87

Swelling of tendons in the carpal tunnel causes nerve compression

Question 88

S&S carpal tunnel

Answer 88

* Tingling and numbness of the thumb, index, middle and ring fingers. * Can also cause pain in the wrist with numbness/tingling * Typically, the patient wakes at night with burning or aching pain and with numbness and tingling and shakes the hand to obtain relief and restore sensation. * Long term compression leads to thenar muscle atrophy and weakness of the thumb and index fingers

Question 89

Treatment carpal tunnel

Answer 89

* Neutral position splinting * Treatment of any underlying disorders * Corticosteroid injection * Surgical decompression

Question 90

Describe 2 tests used in dx of carpal tunnel

Answer 90

Tinel and phalens test

Question 91

Describe tinels test. What is it for?

Answer 91

Dx of carpal tunnel How it’s done: lighting tapping on wrist over median nerve elicits a sensation of tingling or “pins and needles” in the distribution of the nerve. Patho: It is elicited by the tapping (percussion) of an injured nerve trunk at or distal to the site of the lesion. Sensitivity and Specificity: 25-75% and 70-90%, respectively

Question 92

What is phalens maneuvre?

Answer 92

How it’s done: The patient places their flexed elbows on a table, allowing the wrists to fall into maximum flexion. The patient is then asked to push the dorsal surface of their hands together and hold the position for 30-60 seconds. It is considered positive when the patient’s symptoms are reproduced (namely paresthesia) in the distribution of the median nerve. Patho: The pressure on the carpal tunnel increases --> compresses the median nerve between the transverse carpal ligament and the anterior border of the distal end of the radius. Sensitivity and Specitivity: 51-91% and 33-88%, respectively.

Question 93

What are early S&S of ALS?

Answer 93

-Early signs and symptoms: tripping, dropping things, slurring or thick speech, difficulty swallowing, weight loss, decreased muscle tone, DOB, increased or decreased reflexes, uncontrollable laughing or crying, feeling weak, fatigue, muscle cramping or twitching, muscle stiffness or rigidity

Question 94

Describe how symptoms of ALS progress

Answer 94

Over time the muscle weakening will continue to spread throughout the body, eventually causing difficulties with breathing, chewing, swallowing and speaking. - The senses of sight, touch, hearing, taste and smell are usually not affected, and for many people, muscles of the eyes and bladder remain functional until very late in the disease.

Question 95

S&S of spinal form of ALS

Answer 95

60% of people have spinal form of disease * Focal muscle weakness beginning in arms and legs progressing to muscle atrophy, spasticity, and loss of manual dexterity and gait * No associated mental/ sensory/ autonomic symptoms present

Question 96

S&S of ALS with progressive bulbar palsy

Answer 96

ALS with progressive bulbar palsy * Presents with difficulty speaking and swallowing * Peripheral muscle weakness and atrophy occur withing 1-2 years * Poorer response to treatment with mech vent

Question 97

What are 4 classic motor symptoms seen in PD (parkinsons disease)

Answer 97

tremor, rigidity, akinesia/ bradykinesia, postural instability

Question 98

What accounts for the shuffling gait in PD?

Answer 98

* Postural abnormalities (flexion, leaning forward), difficulty walking, and weakness develop as neurodegeneration progresses. Unable to make postural adjustment; festinating gait (short, accelerating steps) is an attempt to remain upright

Question 99

Describe some non- motor impairments of PD?

Answer 99

Non-motor Impairments Psychiatric * Cognitive impairment * Depression, anxiety * hallucinations * Sleep difficulties → wild dreams, excessive day time sleepinesss * Mood disturbances * Decreased motor learning ability * Dementia (advanced stages) Micrographia Autonomic dysfunction * Orthostatic hypotension * Constipation, gastric retention * Urinary retention * Drooling * Increased sweating Decreased sense of smell (olfactory) * Common first symptom → Hx of decreased or changed sense of taste or smell… prior to motor symptoms

Question 100

Complications of PD?

Answer 100

COMPLICATIONS OF PARKINSON’S Freezing phenomenon * Progressive hypokinesia, bradykinesia → akinetic pause in movement * Common when walking * Tend to occur at thresholds (e.g., door frames) Falls * Secondary to postural instability, poor movement amplitude Dystonia → muscles contract involuntarily. * Abnormal tone across joints → disfiguring, painful, posturing * Universal flexion of joints → severely kyphotic posturing * Ultimately results in poor ability to ambulate and ventilate Dementia * Common after prolonged, primarily motor disease (in contrast to Lewy body dementia) * Psychosis, hallucinations (severe) * Progressive (more common in age >70). Further compromise of mental status may occur by the adverse effects of the medication taken to control symptoms NOTE: Despite the various motor symptoms of PD, there is NO WEAKNESS of muscles. This differentiates PD from motor cortex or corticospinal pathway disease

Question 101

What is the diagnostic test for PD?

Answer 101

There is none. It is based on history and clinical presentation. Suspect in anyone with tremor, stiffness, slowness, balance issues, or gait disorders. CT/ MRI should not be routinely used. Trial of dopamine therapy- if it improves symptoms, helps to confirm diagnosis.