Week 10 NEURO pt 1 Flashcards
(153 cards)
1
Q
Facilitates voluntary muscle control of muscles of the face, head and neck via upper motor neurons that synapse with cranial nerve motor nuclei in the pons and medulla.
A
The corticobulbar tract
2
Q
Carries upper motor neuron input to motor nuclei of trigeminal, facial, glossopharyngeal, vagus, accessory and hypoglossal nerves.
A
The corticobulbar tract
3
Q
50% of neurons synapse with lower motor neurons on ipsilateral side.
50% decussate and synapse with lower motor neurons on the contralateral side.
A
The corticobulbar tract.
4
Q
What is the pathway of the corticobulbar tract?
A
Travel to pons and synapse with trigeminal and facial motor nuclei and in the medulla the hypoglossal nucleus and the nucleus ambiguus (vagus nerve, glossopharyngeal nerve).
5
Q
Facilitates voluntary control of skeletal muscles through the body
A
Corticospinal Tract (Pyramidal System)
6
Q
Primary pathway for voluntary, willed motor control.
A
Corticospinal Tract (Pyramidal System)
7
Q
Comprised of massive collection of upper motor neurons with long axons that descend from the cerebral cortex to the spine and initiate and regulate voluntary movement.
A
Corticospinal Tract (Pyramidal System)
8
Q
In regard to the Corticospinal Tract (Pyramidal System) pathway:
In the medullary pyramids,
Approximately 90% of neurons decussate (crossover) to contralateral side – known as (1) _________corticospinal tract in the white matter of the spinal cord.
Approximately 10% of neurons stay ipsilateral and make up the (2) _________ corticospinal tract.
A
(1) lateral
(2) anterior
9
Q
Arise from high up in central nervous system in cerebral cortex
In corticospinal tract, transport signals from cerebral cortex to lower motor neurons
In corticobulbar tract, transport signals from cerebral cortex to synapse with cranial nerve motor nuclei in the pons and medulla
A
Upper Motor Neurons
10
Q
Located in ventral horn grey matter of spinal cord
Transports signals from upper motor neuron to effector muscle to perform a movement
Receives signal from upper motor neuron synapse which then travels from ventral horn to ventral root/ramus out to skeletal muscle
Releases acetylcholine which binds with nicotinic cholinergic receptors on skeletal muscles resulting in muscle contraction
A
Lower Motor Neurons
11
Q
The pathway of the Corticospinal Tract (Pyramidal System) is complex but we are expected to know it. Try to list the steps in which neurons travel through this system.
This is probably just a card to stare at and hope for some retention…
A
Upper motor neuron originates from cerebral cortex
through the internal capsule to the cerebral peduncles in the midbrain
descends through the pons proper
into the medullary pyramids
–Approximately 90% of neurons decussate (crossover) to contralateral side
Approximately 10% of neurons stay ipsilateral and make up the anterior corticospinal tract
then descends into the spinal cord and runs down through anterior or lateral corticospinal tract.
At target level, anterior corticospinal tract decussates prior to synapsing to neuron in the anterior horn of grey matter
Lateral corticospinal tract synapses to neuron in ventral horn of grey matter when they get to appropriate level
Then travels through ventral root into ramus to skeletal muscles
12
Q
Which is CN VII?
A
The facial nerve
13
Q
Is the innervation of CN VII (the facial nerve) motor, sensory, or motor AND sensory?
A
Motor and sensory.
14
Q
What are the functions of CN VII, the facial nerve?
A
Facial expressions
Supplies motor fibres to Lacrimal (tears) and salivary glands
Taste (carries sensory fibres from taste buds of anterior part of tongue
15
Q
Which is CN VIII?
A
CN VIII – Vestibulocochlear (acoustic)
16
Q
Is the innervation of CN VIII (the vestibulocochlear or acoustic nerve) motor, sensory, or motor AND sensory?
A
Sensory
17
Q
What are the functions of CN VIII, the vestibulocochlear nerve?
A
Transmits sense of equilibrium (vestibular branch)
Transmits sense of hearing (cochlear branch)
18
Q
Which is CN IX?
A
CN IX = glossopharyngeal nerve
19
Q
Is the innervation of CN IX (the glossopharyngeal nerve) motor, sensory, or motor AND sensory?
A
Motor and sensory
20
Q
What is the function of CN IX, the glossopharyngeal nerve?
A
Motor fibres serve pharynx and salivary glands (gag and swallow reflex)
Carries signals from pharynx, posterior tongue (taste) and pressure receptors of carotid artery
21
Q
What is the most common type of headache?
A
Tension headache.
22
Q
What are some epidemiological factors of tension-type headache (TTH)?
A
Average age of onset is second decade of life
Affects all genders equally, 31% to 74% of the population
Occurs in 90% of school-aged children
Increased risk with family history
23
Q
What type of headache occurs due to contraction of muscles of the scalp and neck?
Predisposing factors:
-tension/stress
-cervical or back disorders
A
Tension-type headache (TTH).
24
Q
Episodic tension-type headache (TTH) is associated with which pain mechanism and sensory nerves?
A
Peripheral pain mechanism-sensitization of myofascial sensory nerves
25
Chronic tension-type headache (CTTH) is associated with which pain mechanism and cranial nerve?
Associated with central pain mechanism- hypersensitivity of pain fibers from the trigeminal nerve that leads to central sensitization.
26
What is the time course to diagnose a patient with chronic tension-type headache (CTTH)?
Chronic Tension Type Headaches: diagnosed when patient has TTH at least 15 days per month for at least 3 months.
27
These are s/s of which type of headache?
-Mild to moderate bilateral headache with a sensation of a tight band or pressure around the head with onset of pain
-not aggravated by physical activity
-no other associated features
Tension-type headache.
28
What are some treatment options for tension-type headache?
Mild: ice/heat for muscular tension
Mod-severe: NSAIDS, Acetaminophen, ASA, caffeine
Prevention strategies include
-stress reduction, daily exercise, massage, dental appliances for teeth grinding/clenching at night
CTTH: tricyclic antidepressants and behavioral/relaxation therapy
Botox injections are beneficial for some
29
Where would a lower motor lesion occur?
In anterior/ventral horn of spinal cord and motor nuclei of brainstem.
30
Axon from these cell bodies bring impulses from upper motor neurons to skeletal muscles through anterior spinal roots or cranial nerves.
Lesions here impair both voluntary and involuntary movement.
Lower motor neurons.
31
What will you see in terms of muscle tone in a patient with a lower motor lesion?
Hypotonia, flaccidity
32
What types of involuntary movements might you see in a patient with a lower motor lesion?
Fasciculations - muscles rippling or quivering under the skin.
33
How do lower motor lesions affect reflexes?
Hyporeflexia/areflexia
Decreased muscle stretch reflexes.
The plantar reflex is absent.
34
You see the following pattern of muscles weakness? What type of motor lesion do you suspect?
Individual muscles may be affected, mild weakness, marked muscle atrophy.
Can be asymmetrical and may involve one limb in beginning to become generalized w disease progression.
Lower motor lesion.
35
What kind of seizures are notable for EEG changes as both hemispheres of the brain are involved?
Almost all of these types of seizures involve loss/impaired consciousness.
May be preceded by an aura
Generalized seizures.
36
What are the four subtypes of generalized seizures?
Tonic Clonic (grand mal seizures)
Absent seizures (petit mal seizures)
Atonic Seizures (drop seizures)
Myoclonic Seizures
37
What might you see with a tonic clonic (grand mal) seizure?
Generally last one to two minutes
Notable for falls, cries, rigidity (tonicity), jerking (clonicity), with possible cyanosis, and urinary incontinence.
May be preceded by a prodome of unease or irritability (hours or days).
A grand mal seizure is followed by a postictal phase.
38
What might you see with an absent (petit mal) seizure?
Usually last 2 to 15 seconds
Notable for beginning and ending abruptly.
Symptoms noted include staring, eye flutters or eye rolling, and automatisms.
First aid is not required.
39
What might you see with atonic (drop) seizures?
Characterized by abrupt loss of muscle tone, loss of posture, or sudden collapse.
These seizures tend to be resistant to medication.
Protective headgear may be needed.
Generally first aid is not required unless an injury occurs.
40
What might you see with myoclonic seizures?
Characterized by rapid, brief contraction of muscles (sudden jerks or clumsiness), usually on both sides of the body, arm, or sudden jerk of a foot during sleep.
First aid is generally not required.
A single spasm upon transition to sleep is considered normal.
41
What are some general physical characteristics on non-REM sleep?
Begins when the hypothalamus releases inhibitory signals.
Sympathetic tone decreases, and parasympathetic activities increase (remember rest and digest).
Men can experience penile erections; women can experience clitoral engorgement.
Basal metabolic rate decreases from 5-10%.
Pupil constriction occurs.
42
How many stages of non-REM sleep are there?
3
43
What are some characteristics of the
non-REM sleep stage N1?
Brain activity is theta waves (high frequency, low amplitude waves).
Very light sleep, alternating from dozing to wakefulness.
Hypnic jerks, or muscle twitches occur.
Hypnogogic hallucinations occur – false sensory experiences where people often see someone standing in the room or hear their name called, for example.
44
What are some characteristics of the
non-REM sleep stage N2?
Brain activity is still in theta (high frequency, low amplitude waves), but sleep spindles and K-complexes are seen on EEG.
Sleep spindles are brief bursts of high brain activity.
K-complexes are brief spikes in elevation of waves, quickly normalizes.
A theory behind spindles and K-complexes is that information is trying to process but the thalamus is filtering it out to help us remain asleep.
45
What are some characteristics of the
non-REM sleep stage N3?
Brain activity is delta waves (low frequency, high altitude waves).
Deep sleep, very difficult to wake from N3.
Growth hormones are released, cell repair is underway.
Parasomnias (sleep disorders) occur, such as sleep walking/talking, bed wetting.
46
What are some characteristics of the Rapid Eye Movement (REM) sleep stage?
Brain activity resembles wakefulness, or theta in N1.
Most dreaming occurs in REM – these are the dreams we are most likely to remember.
AKA paradoxical sleep. The paradox is that we have a very active brain but also have muscle paralysis.
We can experience irregular heart rate, resp rate, and a change in body temperature.
This stage is important for memory and learning. If we learned something new that day and then did not have a great sleep with enough REM, we may have difficulty retaining that information.
47
The cycle typically cycles through
N1-> N2-> N3-> REM-> N1 or 2-> REM-> N1 or 2-> REM etc.
The first REM stage typically occurs after the first hour of sleep.
How many cycles of sleep are recommended, or 'typical' of a good night's sleep?
4-6
48
Specific areas of the brain are responsible for different stages of our sleep cycle. The areas are:
-hypothalamus
-pontine reticular formation
-thalamocortical network
-pons and mesencephalon
What does each area influence in terms of sleep?
Hypothalamus: Major sleep centre. Secretes the neuropeptides acetylcholine and glutamate that promote wakefulness, and prostaglandin D2, adenosine, melatonin, serotonin, l-tryptophan, GABA and growth factors which promote sleep.
Pontine reticular formation: Mainly responsible for creating REM sleep.
Thalamocortical network: Projections produce non-REM sleep.
Pons and Mesencephalon: Control REM sleep through REM-on and REM-off neurons.
49
This cranial nerve is a special sensory nerve which carries the signals for vision
CN II – Optic
50
This cranial nerve has somatic and visceral motor functions and is responsible for movement of the extraocular muscles – which direct the eyeball, movement of the eyelid, iris and ciliary body
CNIII – Oculomotor
51
This cranial nerve is a special sensory nerve which carries the signals for the sense of smell
CN1 – Olfactory
52
This cranial nerve had the somatic motor function of controlling motor fibers to lateral rectus muscle and proprioceptor fibers from the same muscle to the brain
CN VI – Abducens
53
This cranial nerve has the somatic nerve function of providing proprioceptor and motor fibers for superior oblique muscle (extraocular muscle) of the eye
CN IV – Trochlear
54
This CN has both somatic motor and sensory functions, It:
Provides motor and sensory impulses for the face
Conducts sensory impulses from the mouth, nose, surface of the eye, and dura mater
Contains motor fibres that stimulate chewing muscles
CN V - Trigeminal
55
This cranial nerve is a motor nerve, responsible for the Sternocleidomastoid (turning the head) and trapezius (shrugging your shoulders) muscles. As well as muscles of the soft palate, pharynx, and larynx (plays a role in swallowing and breathing)
CN XI – Accessory
56
This cranial nerve has both motor and sensory functions - carries sensory and motor signals to the pharynx, larynx and esophagus (responsible for coughing, sneezing, swallowing and vomiting)
Parasympathetic motor fibres supply smooths muscle of abdominal organs (responsible for digestion, HR and RR)
Somatic sensation from the skin behind the ear, outer ear canal and throat.
CN X – Vagus
57
This cranial nerve has only motor functions and is responsible for the muscles of the tongue responsible for speech
CNXII – Hypoglossal
58
List the cranial nerves I – XII
List the cranial nerves I – XII
I – Olfactory
II – Optic
III – Oculomotor
IV – Trochlear
V – Trigeminal
VI – Abducens
VII – Facial
VIII – Vestibulocochlear
IX – Glossopharyngeal
X – Vagas
XI – Accessory
XII – Hypoglossal
(Ooh, ooh, ooh, to touch and feel very good velvet, always heaven.) or whichever mnemonic you prefer
59
List which nerves are sensory, motor or both
Some say marry money, but my brother says big brains matter more.
I – Olfactory - SENSORY
II – Optic - SENSORY
III – Oculomotor - MOTOR
IV – Trochlear - MOTOR
V – Trigeminal - BOTH
VI – Abducens - MOTOR
VII – Facial - BOTH
VIII – Vestibulocochlear - SENSORY
IX – Glossopharyngeal - BOTH
X – Vagas - BOTH
XI – Accessory - MOTOR
XII – Hypoglossal - MOTOR
60
Which headache is characterised by a headache lasting 4-72 hours with 2 of the following: unilateral head pain, throbbing pain, pain worsening with activity, moderate or severe pain intensity; and at least one of the following: nausea and/or vomiting, or photophobia and phonophobia.
Migraines
61
Why are women thought to have a higher incidence of migraines than men?
Biologic sex: higher in females: 12% of women; 5% of men in Canada
In women, migraines most frequently occur before & during menstruation; decreased during pregnancy & post menopause. The cyclic withdrawal of estrogen & progesterone may trigger attacks.
62
What is the age of onset for migraines?
Childhood, teens and young adults, more common in 30s-40s
63
Migraines increase a person's risk for which other health problems?
Epilepsy
Depression & anxiety disorders
Cardiovascular disease
Stroke
64
What are some possible triggers for a migraine?
Too tired or oversleeping
Missed meals
Overexertion
Weather changes
Stress… or relaxation from stress
Hormonal changes (menstruation)
Excess afferent stimulation (ex. bright lights, strong smells)
Chemicals (alcohol, nitrates)
65
The patho of migraines is complex and not well understood, what are some of the general theories?
Current theories include neurological, vascular, hormonal, and neurotransmitter components.
66
What are the 4 phases of a migraine?
Premonitory phase: ⅓ of persons have premonitory symptoms hours to days before onset of headache. Symptoms include: tiredness, irritability, loss of concentration, stiff neck, food cravings.
Migraine aura: ⅓ of migraines come with aura symptoms at least some of the time; may last up to 1 hour. Aura symptoms can be visual, sensory, motor.
Headache phase: throbbing pain usually begins on 1 side and spreads to include the entire head. May be accompanied by fatigue, N&V, dizziness. There may be hypersensitivity to anything touching the head. Symptoms last 4-72 hours (usually about 1 day).
Recovery phase: irritability, fatigue, or depression; may take hours or days to resolve.
67
Describe the symptoms of a migraine
Often preceded by symptoms such as:
Irritability
Depression
Fatigue
Headache symptoms:
Pounding or pulsating
Typically localized to one side of head (but can be bilateral)
Lasts hours → days
Additional symptoms:
N & V
Irritability
Photophobia (discomfort with lights)
Phonophobia (discomfort with sound)
Osmophobia (discomfort with smells)
Most migraines do not have aura
But 25-30% of migraine DO have aura
Aura → experiencing strange smells, lights, visual disturbances, or even hallucinations before the onset of migraine
68
Outline the diagnostic criteria for migraines
≥ 5 attacks → lasting 4-72 hours
≥2 of the following:
One-sided throbbing quality
Moderately severe pain
Worsening with physical activity
≥ 1 of the following:
Nausea / vomiting
Photophobia (light sensitivity)
Phonophobia (sound sensitivity)
69
Summarize treatment for mild and severe migraines
Mild/Moderate: NSAIDS, Tylenol
Moderate/Severe: Triptans, dopamine agonists (metoclopramide, chlorpromazine), dexamethasone, antihypertensives (beta-blockers, CCB, ACEI, ARBs), antidepressants (tricyclic antidepressants, SNRIs), anticonvulsants
70
What constitutes chronic migraines? What are they associated with?
Begin as episodic migraines that increase in frequency over time.
Occurs at least 15 days in a month for more than 3 months
Can occur daily or on a near-daily basis)
Associated with:
Overuse of analgesic migraine medications (sometimes called rebound headaches)
Obesity
Caffeine overuse.
71
Which headache type is characterized by attacks of severe unilateral pain with ipsilateral cranial autonomic symptoms and/or restlessness/agitation?
Cluster headaches
72
What are some factors that predispose individuals to cluster headaches?
Male
Most commonly age 20-40 at onset
Family history
Smoking/secondhand smoke
Head trauma
73
What is the patho theory for cluster headaches?
Complex and not completely understood.
Most common theory: Characterized hypothalamic activation with secondary activation of the trigeminal-autonomic reflex, probably via a trigeminal-hypothalamic pathway.
Vascular theory: neurogenic inflammation within the walls of the cavernous sinus due to obliteration of venous outflow that injures the traversing trigeminal c-fibers and sympathetic fibers along the intracranial internal carotid artery
74
Describe the time course for cluster headaches
15 minute – 3 hour duration. May occur from every other day, up to 8 times per day. Frequently recurring attacks occur in a cluster or bout and are separated by periods of remission – where patients are asymptomatic often for months
Episodic cluster bouts – The episodic form affects 80 to 90 percent of patients with cluster headache. It is characterized by alternating periods of attacks and remission. Bouts may last from 7 days to 12 months if untreated. Periods of remission last at least three months, during which time patients are usually asymptomatic.
Chronic cluster bouts – Patients with the chronic form of cluster headache report either continual attacks (persisting bout) or report brief remissions of less than three months. Chronic cluster headache may arise de novo or evolve both from and to the episodic type. Cluster headache is considered chronic once a bout persists for a year without remission.
75
Describe the headache associated with cluster headaches
Severe sharp or stabbing pain
Commonly in the periorbital or temporal regions
Strictly unilateral (although can shift to the other side in separate attacks in 15% of patients)
76
Outline some of the autonomic symptoms associated with cluster headaches
Typically occur only during acute attack.
Ipsilateral to the headache and may include ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, and/or nasal congestion. Sweating and increased cutaneous blood flow. Some report cutaneous allodynia.
Some patients with cluster have chronic signs of sympathetic paralysis such as miosis and ptosis that transiently intensify during acute attacks
In rare cases, sympathetic disturbances persist on the previously affected side of the face in patients whose cluster headache has switched sides
77
Outline Acute. Transitional and prophylactic cluster headache treatments
Acute: triptans (sumatriptan, zolmitriptan); 100% O2 through non-rebreather
Transitional: short term prednisone, DHE (dihydroergotamine), occipital nerve block with corticosteroid
Prophylactic: verapamil, lithium, topiramate
78
Match the headache description with the headache type
1. Migraine
2. Cluster headaches
3. Tension-type headaches
A. Unilateral (or sometimes bilateral) throbbing or pulsatile headache that worsens with activity and lasts 4-72 hours
B. Bilateral, band-like non-throbbing headache with no associated features, lasting 4-6 hours
C. Unilateral, stabbing periorbital headaches with associated autonomic symptoms, lasts 15 minutes – 3 hours
1. Migraine - A. Unilateral (or sometimes bilateral) throbbing or pulsatile headache that worsens with activity and lasts 4-72 hours
2. Cluster headaches - C. Unilateral, stabbing periorbital headaches with associated autonomic symptoms, lasts 15 minutes – 3 hours
3. Tension-type headaches - B. Bilateral, band-like non-throbbing headache with no associated features, lasting 4-6 hours
79
Which headache type sometimes has 100% oxygen via a non-rebreather as a treatment?
Cluster headaches
80
Impaired ability to estimate distance in muscular action.
Tendency for limb movements to overshoot or undershoot a target
Dysmetria
81
Impairment of the ability to make movements exhibiting a rapid change of motion that is caused by cerebellar dysfunction
Dysdiadokokinesis
82
Impairment of the ability to perform smoothly coordinated voluntary movements
Due to central nervous system disorders and injuries and not due to muscle weakness
Ataxia
83
Loss or impairment of the ability to execute complex coordinated movements without muscular or sensory impairment
Apraxia
84
An impaired ability to comprehend or express language in its written or spoken form
Usually the result of a stroke, head injury, or infection
Aphasia
85
Difficulty with swallowing
Dysphagia
86
Loss of the ability to comprehend the meaning or recognize the importance of various forms of stimulation that cannot be attributed to impairment of a primary sensory modality.
Agnosia
87
Loss of or impaired ability to smell
Anosmia
88
Extreme slowness of movements and reflexes
Can be caused by Parkinson’s disease or antipsychotic drugs
Bradykinesia
89
Abnormally small handwriting or handwriting that becomes progressively smaller that is characteristic especially of Parkinson’s disease
Micrographia
90
Extrapyramidal includes all motor pathways except the pyramidal system. There are two types of motor dysfunction which result in movement or posture disturbance without significant paralysis. What are these motor dysfunctions called?
Basal cell ganglia motor syndromes and cerebellar motor syndromes
91
Which extrapyramidal syndrome results from imbalance of dopaminergic and cholinergic activity in corpus striatum. Excess of cholinergic activity=akinesia and hypertonia
Excess of dopaminergic activity=hyperkinesia and hypotonia
Basal cell ganglia motor syndromes
92
What are the symptoms associated with cerebellar motor syndromes?
Ataxia and other symptoms affecting coordination of movement
93
In extrapyramidal lesions, what can you expect to see for involuntary movement, reflexes and patterns of muscle weakness?
Presence of tremor, chorea, athetosis, or dystonia
Normal or slightly increased tendon reflexes.
Absent plantar reflexes
Plastic rigidity (equal throughout movement) or intermittent cogwheel rigidity (generalized but predominantly in flexors of limbs and trunk)
Hypotonia, weakness, and gait disturbances in cerebellar disease
94
Provide a general definition of MS
Multiple sclerosis is is a chronic immune-mediated inflammatory disease involving degeneration of CNS myelin, scarring, and loss of axons.
95
Who is most likely to be diagnosed with MS?
Canada has one of the highest rates of MS in the world
Approx. 90,000 Cdn’s living with the disease, or 1 in 500
Onset between 20 and 50 years of age
More common in women
Men may have more severe prognosis
Prevalence higher in norther latitudes
96
What are additional risk factors for MS?
Risk Factors
Smoking
Vit. D deficiency
Obesity
Infection including Epstein Barr virus
Genetic Factors
97
Give a brief overview of the patho of MS
Not well understood
Likely autoimmune myelin destruction triggered (viral, environmental, metabolic) in genetically susceptible individuals
Auto reactive T and B cells cross the blood brain barrier and attack the myelin sheaths in the CNS, resulting in inflammatory response leading to inflammatory response and eventual plaque formation and scarring. Loss of myelin disrupts nerve signals, resulting in neuron death and brain atrophy/permanent disability. Spinal MS can also occur, without brain lesions.
98
Describe the time course of MS
Chronic and progressive
Intermittent exacerbations: lasting at least 24 hours; complete recovery after first attack is common but typically converts to MS within five years
Recurrent relapses and remissions
99
What are common signs and symptoms of MS?
Most common initial symptoms are paresthesias of the face, trunk, or limbs; weakness; impaired gait; visual disturbances; or urinary incontinence, indicating diffuse CNS involvement.
Cerebellar and corticospinal involvement presents as nystagmus, ataxia, and weakness with all four limbs involved. Intention tremor and slurred speech may also occur.
Visual impairment is associated with optic neuritis.
Onset, duration, and severity varies.
Disease exacerbations (i.e. relapses or flares) are temporary occurrence or worsening of symptoms. Varied. Mild or serious, days to weeks. Can be followed by progressive symptoms such as paresthesia, difficulty speaking, ataxia, or visual changes. Trauma, emotional stress, pregnancy can be precipitating factors/triggers to exacerbations.
Painful sensory events, spastic paralysis, and bowel and bladder incontinence are common with spinal involvement.
Early cognitive changes are common and may include poor judgement, apathy, emotional lability, and depression.
100
What are the four different types of MS
MS Society of Canada identifies 4 types of MS:
Clinically Isolated Syndrome: earliest form of MS, refers to a single episode of neurological symptoms suggestive of multiple sclerosis
Relapsing-remitting MS: unpredictable but clearly defined relapses (also known as attacks, exacerbations or flare-ups) during which new symptoms appear or existing ones get worse.
Secondary progressive MS: progressive worsening and fewer relapses.
Primary progressive MS: slow accumulation of disability, without defined relapses
101
What components go into an MS diagnosis?
Clinical history and neurological exam
MRI (most sensitive): detects demyelinated plaques and monitors disease.
Lumbar puncture: constantly elevated levels of CSF IgG and Oligoclonal IgG bands on electrophoresis are common in persons with MS
Evoked potentials (measures the speed of nerve impulse conduction): detects decreased conduction velocity in visual, auditory, and somatosensory pathways.
A diagnosis of MS must include evidence of disease activity separated in time (lesions that formed at different points in time) and space (lesions in at least two separate areas of the CNS).
102
Who is the most appropriate person to prescribe MS therapies?
Referral should be made to a neurologist who specialises in MS
103
Outline some of the pharmacological management options for MS
Disease-modifying drugs: suppress the immune system to slow progression of MS, decreasing the frequency and severity of exacerbations, and reducing MS-related plaques; requires continuous monitoring d/t increased risk of infection.
Short-term steroid use (e.g., methylprednisolone or prednisone for three to five days) may shorten a period of exacerbation.
Plasma exchange: for people who do not respond to corticosteroids
Symptom control medications
104
Outline some non-pharm management components for MS
Diet: Many special diets have been proposed as treatments, but none have been proven to prevent MS or affect the way it may develop. MS specialists recommend that people follow the same high fiber, low fat diet recommended for all adults.
Exercise/rehab therapy: In addition to improving overall health, aerobic and strength exercise reduce fatigue and improve bladder and bowel function, strength, balance, mobility and mood. Stretching exercises reduce stiffness and increase mobility.
Stress Management (stress may exacerbates symptoms)
Vit. D: Aside from its role in promoting calcium absorption and overall good bone health, vitamin D has also been shown to have a direct effect on the immune system. As a result, researchers are determining the relationship between inadequate vitamin D and the risk of MS, as well as the effect of vitamin D intake in treating MS
105
In Carpel Tunnel Syndrome, which nerve is compressed?
The median nerve
106
What usually causes carpel tunnel syndrome?
Often linked to occupational repetitive movements related to wrist flexion/extension, holding the wrist in an awkward position, or strong gripping of objects. Typing is a common cause
107
What are the expected signs and symptoms of Carpel tunnel syndrome?
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
108
What are the treatment options for carpal tunnel syndrome?
Neutral position splinting
Treatment of any underlying disorders
Corticosteroid injection
Surgical decompression
109
What are the names of the two tests used for carpel tunnel syndrome testing? How are they performed?
PHALEN’S MANEUVER:
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 Specificity: 51-91% and 33-88%, respectively.
TINEL’S SIGN:
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
110
Cubital tunnel syndrome is caused by compression of which nerve? Where is this tunnel located?
The ulnar nerve
Located in the posterior aspect of the elbow
Can also be caused by direct trauma to the nerve
111
What are common causes of cubital tunnel syndrome?
Often caused by leaning on the elbow or prolonged and excessive elbow flexion.
112
What are signs and symptoms of cubital tunnel syndrome?
Numbness and tingling along the ring and little fingers, and ulnar aspect of the hand
Can present as elbow pain
Long term compression causes weakness of intrinsic muscle of the hand and flexors of the ring and little finger
Chronic compression leads to ulnar hand claw due to muscle imbalances
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Match the type of generalized seizure to their descriptions
A. tonic-clonic
B. atonic
C. myoclonic
D. absence
1. musculature stiffens, then intense jerking as trunk and extremities undergo rhythmic contraction and relaxation
2. sudden, brief contractures of a muscle or group of muscles
3. brief loss of consciousness with little or no loss of muscle tone; may experience 20 or more episodes/day, lasting about 5-10 seconds each, may have minor movement such as lip smacking, twitching of eyelids
4. sudden momentary loss of muscle tone, drop attacks
A. tonic-clonic - 1. musculature stiffens, then intense jerking as trunk and extremities undergo rhythmic contraction and relaxation
B. atonic - 4. sudden momentary loss of muscle tone, drop attacks
C. myoclonic - 2. sudden, brief contractures of a muscle or group of muscles
D. absence - 3. brief loss of consciousness with little or no loss of muscle tone; may experience 20 or more episodes/day, lasting about 5-10 seconds each, may have minor movement such as lip smacking, twitching of eyelids
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Define Status Epilepticus
Continuing or recurring seizure activity in which recovery from seizure activity is incomplete; seizure activity can last 30 mins or more; medical emergency that requires immediate intervention
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Define Febrile Seizure
Seizure activity associated with a high body temperature but without any serious underlying health issue, occurs most often in children between ages of 6 months and 5 years
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What is the main hormone which promotes sleep?
Melatonin
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What are other factors (neurotransmitters) which promote sleep?
Neurotransmitters: prostaglandin D2, adenosine, serotonin, l-tryptophan, GABA, pro-inflammatory cytokines (mediate sleepiness and lethargy associated with infectious illness)
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Which neurotransmitters are involved in wake behaviours?
Wake behaviour: neurotransmitters involved: Hypocretins (orexins), glutamate, acetylcholine, norepinephrine, dopamine, histamine
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What is hydrocephalus?
Refers to various conditions characterized by excess CSF in the ventricles, subarachnoid space, or both.
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What are potential causes of hydrocephalus?
Causes include:
Increased CSF production
Obstruction within the ventricular system
Defective CSF reabsorption
interference with CSF flow.
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What are the types of hydrocephalus
Noncommunicating hydrocephalus – obstruction within the ventricular system. Occurs most often in children.
Communicating hydrocephalus – faulty resorption of CSF from the subarachnoid space. Most common in adults.
Acute hydrocephalus: Presents with signs of rapidly developing increased ICP.
Normal-pressure hydrocephalus (dilation of the ventricles without increased pressure):
Develops slowly – individual or family noting declining memory and cognitive function.
Hallmark symptoms: remember “3 Ws” Wet, Wobbly, Wacky
Wet – Urinary incontinence
Wobbly - Unsteady, broad-based gait (small, wide, slow steps, unable to pick up feet) with a history of falls
Wacky – Dementia - slow thought processes, reduced concentration, memory problems, behaviour changes
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Name two CN V lesions causing facial pain
Trigeminal neuralgia, herpes zoster opthalmicus
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What is trigeminal neuralgia
* Recurrent, brief, shock like pain alone the distribution of CNV
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Patho of trigeminal neuralgia
* Exact pathophysiology unknown; thought to be caused by compression of trigeminal nerve by vasculature near exit from pons in brainstem. Can also be caused by MS, tumours, or other. This results in nerve demyelination and atrophy, leading to hyperexcitability and abnormal nerve signalling. Central sensitization (abnormal state of responsiveness to pain) may also be a component of trigeminal neuralgia.
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Clinical manifestations trigeminal neuralgia
o Spontaneous or triggered sudden, brief, unilateral, severe stabbing pain following the distribution of one or more branches of the trigeminal nerve (
o Pain described as stabbing, electric shock like, burning
o Recurrent episodes, each lasting seconds to two minutes, followed by a refractory period (seconds to minutes)
o Pain most commonly experiences in V2 and V4 (maxillary and mandibular) branches of CN V
o May see muscle spasms with severe pain
o Triggers can be innocuous and include touching the face, brushing teeth, talking, eating. The trigger zone follows the distribution of trigeminal nerve
o May be associated with autonomic symptoms (i.e., lacrimation)
o Approximately 50% of patients also have aching/ burning/ low intensity continuous pain in the same area as the episodic pain
o Bilateral pain is very uncommon
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What is herpes zoster opthalmicus
* Viral involvement of ophthalmic division of CNV
* After primary infection, varicella zoster virus is established in the sensory ganglion of CNV. Latent varicella zoster virus can become reactivated, and travels along CNV
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Clinical manifestations herpes zoster opthalmicus
o May be preceded by fever, fatigue, malaise, headache
o Unilateral dermatome forehead rash (maculopapular or vesicular rash along the first branch of the trigeminal nerve)
o Painful inflammation of eye tissues (usually anterior) (keratitis, uveitis, retinitis) *ophthalmic emergency
o Pain is burning, shooting, can be accompanies by paresthesias
o May result in postherpetic neuralgia
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What is Bells palsy
* Unilateral facial nerve palsy (weakness or paralysis) (CNVII lesion)
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Patho of Bells palsy?
* Exact etiology unknown, likely caused by inflammation of CNVII causing compression (CNVII travels through narrow canals in temporal bone and exits via the stylomastoid foramen). May be due to reactivation of HSV in CNVII, or due to an autoimmune response. Inflammation/ compression of CNVII leads to ischemia and degeneration, resulting in impaired signalling and transmission of motor impulses. Ipsilateral weakness or facial paralysis will result (along with loss of sensation in anterior tongue)
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Clinical manifestations Bells palsy?
* Clinical manifestations:
o Acute onset of unilateral facial weakness or paralysis
* Impaired forehead wrinkling
* Inability to close eye of affected side, drooping of eyelid
* Mouth drooping to affected side/ inability to smile
* Flattened nasolabial fold
* Can be associated with involuntary movements (synkinesis)
o Facial paresthesia
o Drooling
o Decreased tearing or abnormal lacrimation with eating
o Hypersensitivity to sound (hyperacusis)
o Ear pain
o Vesicular rash in ear (suggestive of Herpes Zoster cause)
o Pain associated with facial palsy
o Change in sensation of taste (anterior tongue)
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Define an upper motor neuron lesion
-The result of damage to descending motor pathway at cortical, brainstem, or spinal cord levels. Paresis (weakness) or paralysis (loss motor fx) also known as spastic paresis/paralysis.
-Paresis or paralysis of UMN is associated with pyramidal motor syndrome.
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Causes of UMN lesions?
-Causes of UMN syndrome can be neoplasm, trauma, inflammation. Other causes listed below by location.
-Motor cortex caused by birth injuries (cerebral palsy of childhood).
-Internal capsule – vascular lesions like CVA.
-Brainstem- demyelinating disease like MS, vascular lesions, or degenerative diseases like Parkinson's.
-Spinal cord- demyelinating disease
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What is the muscle tone that is seen in UMN lesions?
Muscle overactivity, Hypertonia/spasticity
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Are there any involuntary movements with UMN lesions?
- Absence of involuntary movement
-Clonus/spasm - occurs often due to loss of higher motor center control.
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What is characteristic of reflexes in UMN lesions?
hyperreactive.
Increased muscle stretch reflexes- clasp knife spasticity, resistance to passive flexion
-Loss abdominal reflex. -Hoffmann signs
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Are plantar reflexes present in UMN lesions?
yes
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Describe the pattern of muscle weakness in UMN lesions
-Muscle groups affected, mild weakness, minimal disuse muscle atrophy.
-Spinal shock is temporary loss of spinal cord fx below lesion (below level of pons)-characteristics: complete flaccid paralysis, absence of reflexes, and marked bowel/bladder function disturbance, hypotension due to loss of sympathetic tone. Major factor is sudden destruction of efferent pathways.
-Lesion above pons- hand and arm muscles greatly affected. Paralysis rarely involves all muscles on one side of body.
-Paralysis associated with pyramidal motor syndrome rarely remains flaccid. Gradual return of reflexes marks the end of spinal shock. Reflexes become hyperactive and muscle tone increases greatly.
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The spinothalamic tract is responsible for _______________
Sensation
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The lateral spinothalamic tract is responsible for what kind of sensory information?
pain and temp
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The anterior spinothalamic tract is responsible for what kind of sensory information?
touch and pressure
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What is the medial leminiscal path responsible for?
fine touch and proprioception
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Name the 3 types of somatic sensory receptors
Touch & proprioception à mechanoreceptors
Pain à nociceptors
Temperature à thermoreceptors
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Describe what kind of sensory information the following somatosensory fibers carry:
Non myelinated fibers type C
Small myelinated fibers Type A
Large myelinated fibers Type A
Non myelinated fibers à type C – slowest, burning pain, hot temp,
Small myelinated fibers à Type A delta – faster than C – sharp pain (gross touch, cold temp)
Large myelinated fibers à type A alpha, A beta fibers – fastest fibers, proprioception, vibration, fine touch
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Describe focal partial seizures
Can be simple or complex
* Partial (focal) seizures generally only involve one portion of the brain (either left or right cerebral hemisphere)
* They are the most common type of seizure
* May be accompanied by visual or auditory hallucinations
* Aura is common
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How do simple partial seizures differ from complex partial seizures?
Simple partial seizures:
* Not associated with altered consciousness or loss of consciousness.
* Common SPS includes jerking of a limb and may be preceded by an aura, including epigastric discomfort, fear, or unpleasant smells.
Complex partial seizures
* Notable for impaired consciousness.
* Confusion, fatigue, and headaches may follow a CPS.
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What is cerebrospinal fluid? (CSF)
Cerebrospinal fluid (CSF) is a clear, plasma-like fluid (an ultrafiltrate of plasma) that bathes the central nervous system (CNS). It occupies the central spinal canal, the ventricular system, and the subarachnoid space.
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What creates CSF
Ependymal cells (line the ventricles of brain and center of spinal cord)
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What secretes CSF
choroid plexus
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How much CSF is produced daily
400-600mls
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How does hydrocephalus result?
* Disequilibrium in synthesis and resorption or obstruction of circulation results in CSF accumulation and raised intracranial pressure called hydrocephalus
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How do you examine CSF?
lumbar puncture
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Where is CSF produced?
* CSF is produced mainly by a structure called the choroid plexus in the lateral, third and fourth ventricles.
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Describe flow of CSF
* CSF flows from the lateral ventricle to the third ventricle through the interventricular foramen (also called the foramen of Monro).
* The third ventricle and fourth ventricle are connected to each other by the cerebral aqueduct (also called the Aqueduct of Sylvius).
* CSF then flows into the subarachnoid space through the foramina of Luschka (there are two of these) and the foramen of Magendie (only one of these).
* Absorption of the CSF into the blood stream takes place in the superior sagittal sinus through structures called arachnoid villi.
