Nuero Block I: Diseases Of The Nerve Flashcards
How many pairs of spinal nerves are there
31 pairs
8 cervical 12 thoracic 5 lumbar 5 sacral 1 coccygeal
What are the basic parts of the neuron
The cell body, axon, and dendrites
What is the recieveing portion of the neuron
The dendrite
What part of the neuron propagates impulses to other neurons
The axon
Where do axons arise from
Typically arises from an elevation in the cell body called the axon hillock (= small hill)
Where is the trigger zone on an axon
Impulses (action potentials) generally arise in the trigger zone, the junction of the hillock and initial segment
What class of drug is lidocaine and Marcaine
NA+ channel blockers
Where are Schwann cells located
They are the myelin sheath of the peripheral nerves
Where are oligodendrocytes located
They are the myelin sheath of the CNS
What are the three steps to Dz of the spinal cord
Identify where the lesion is
Identify the cause
Determine proper Tx
What are the seven key questions for dz of the spinal cord
pt approach
What systems are involved
What is the distribution of weakness
What is the nature of sensory involvement
Is there upper neuron involvement
What is the time of S/s
Is there evidence of hereditary neuropathy
Are there associated medical condition s
Wrist drop with weakness in thumb aBduction and finger extension is a sign of neuropathy where
The radial nerve
Sensory loss of the dorsal web space betweeen the thumb and index finger is neuropathy where
Radial nerve
What is the Tx approach to radial neuropathy
Cock up wrist and finger splints
Followed by physical therapy
What is the nerve compression responsible for Carpal Tunnel
Median nerve compression
Numbness in the thumb, index, and middle finger, with aching pain in the hand and forarm that is worse at night…
Carpal tunnel
What is tinel sign
A sing of nerve compression, taping on the nerve leads to tingling sensations through the dermatomes
What is a positive phalens sign
A PE sign for carpal tunnel
What is the Tx approach to CTS
U/s of the median nerve to assess for swelling
EDX: sensory delay before motor delay
Tx: Activity mod. NSAIDs Wrist splint worn at night Methylprednisosne injections
And possible surgical decompression
Parasethisa and tingling of the medial hand, and either the 4th or 5th fingers is compression of what nerve
Ulnar nerve
cubital tunnel syndrome
What are the S/s of cubital tunnel syndrome
decreased sensation in ulnar distribution
Tinel’s sign at the elbow
Froment Sign
postive tinsels sign at the elbow indicates what neuropathy
Compression of the ulnar nerve
What is the Tx approach to Cubital tunnel syndrome
(ulnar nerve compression)
EDX: slowing of ulna motor NCV across the elbow
U/S: swelling of the ulnar nerve near the elbow
Tx: Activity mod Elbow pads Splints Possible surgery
What is meralgia parenthetica
Compression of the lateral femoral cutaneous nerve
Common in obese, DM, and pregnant pts
MERICA= Meralgia
What anatomical position relieves meralgia parenthetica
Sitting
What is the Tx approach to Meralgia paresthetica
Wt loss
Lidoderm patch
NSAIDS
And Neuropathic pain meds
What are the 1st line medication for the Tx of painful sensory neuropathies
Lidoderm TCA- amitryptyline or notriptyline Gabapentin Pregabalin Duloxetine
What are 2nd line agents for Tx of painful sensory neuropathies
Carbamazepine
Phynetoin
Venlafaxine
Tramadol
What are the S/s of a B12 deficiency
Distal symmetric numbness and gait instability with distal weakness
Usually hands numb first
-Harrison’s but Current does not differentiate
GI S/Sx: diarrhea, glossitis, anorexia
PE: Decreased vibratory sensation, hyperreflexia, absent Achilles reflex, gait issue
What is the Tx approach to B12 deficiency
IM injection q weekly x 1 month
Then q month
A B12 deficiency deficits permanent?
50% of pts with have some perm. Neuro deficit
What is the most common complication of DM
Diabetic neuropathies
What is the most common form of DM neuropathy
Diabetic distal symmetric sensory and Sensorimotor Polyneuropathy (DSPN)
What is the TX approach to diabetic neuropathy
Tight glycemic control Pain control (examples): Tricyclic antidepressants Gabapentin Serotonin/norepinephrine reuptake inhibitor Capsaicin cream
A pt that presents with a stocking-glove pattern of neuropathy.. suspect
DM (DSPN)
A pt with otro static HOTN, sweating disturbances, excercse intolerances, bladder dysfunction of ED, with DM suspect
DM neuropathy
What is the number one agent of neuropathies in HIV infected pts
CMV
What is the most common S/s of Lyme Dz neuropathy
facial neuropathy ( bilateral unlike Belsy palsy)
What are the biopsy result in Lyme disease neuropathy
Axon degeneration w/ perivascular inflammation
What is the Tx for Lyme Dz neuropathy
Doxy
A pt presents with severe pain along a dermatomes followed by a vesicular rash.. think
HVZ ( herpes zoster) - a peripheral neuropathy
What is the Tx approach to shingles
Within 72 hours- acyclovir, ect
Reduce pain
What is the most common cause of peripheral neuropathy in Asia, Africa, and South America
Leprosy aka Hansens Dz
A pt that presents with tuberculoid and lepromatous lesions… think
Hansens/ Leprosy
Where is neuropathy most common in leprosy
To the ears and distal limbs
What is the confirmatory lab for leprosy
Acid fast bacillus in skin lesions (( biopsy)
What are the complications of leprosy
Anesthesia, motor d/o, kidney failure, hepatomegaly, and secondary amyloidosis
WHO ecommended Tx of leprosy/ Hansens Dz
Lepromatous: Rifampin 600mg plus Clofazimine 300mg once a month (supervised) AND Dapsone 100mg plus Clofazimine 50mg daily for 1-2 years
Tuberculoid: Rifampin 600mg once a month (supervised) and Dapsone 100mg daily (unsupervised) for 6 months
What is the most common type of hereditary neuropathy
Charcot-Marie-tooth
What is the most common presentation of Charcot-Marie-tooth
Foot drop
A pt that presents with distal weakness, that defines in the legs then spreads to the hands and forearms, has inverted champagne bottle legs (atrophy), Depressed or absent DTRs.. think
Charcot-Marie-tooth
CMT type one distinction
Charcot-Marie-Tooth disease
CMT Type 1 (most common): characterized by demyelination on electrodiagnostic
What is the Tx approach to Charcot-Marie-tooth
Physical and Occupational Therapy
AFO – foot drop
And in late stages surgical intervention to treat foot deformity if unable to manage conservatively
What is HSAN
Hereditary Sensory and Autonomic Neuropathy
Autosomal dominant disease involving progressive degeneration of small myelinated and unmyelinated nerve fibers.
A pt presents with distal sensory loss ( burning, aching, knife like pain) with deep dermal ulcers, recurrent OA, foot and hand deformities, w/ bladder dysfunction and reduced sweating in the feet… think
HSAN
What is familial amyloid polyneuropathy
Mutation in the genes for transthyretin that leads to
- Insidious onset of numbness and painful paresthesias
- Early involvement on the autonomic nervous system
- Cardiomyopathy leading to cardiac failure
What is the Tx approach to Familial amyloid polyneuropathy
Liver transplant
What is refsums Dz
Autosomal recessive Dz
With onset in infancy to early adulthood
Earliest s/s night blindness
What is the earliest s/s of refsums dz
Night blindness
What is the classic tetrad of Refsums
Peripheral neuropathy
Retinitis pigmentosa (Bone spicules in the eye)
Cerebellar ataxia
Elevated CSF protein concentration
What is the Dx criteria for Refsums
Elevated levels of phytanic acid in the serum and urine
What is the Tx approach to refsums
Avoid dietary sources of phytanic acid
Plasmaphoresis
What is the most common variant of Guillian-barre syndrome
Acute Inflammatory Demyelinating Polyradiculoneuropathy
What are the precipitation fxs that lead to Guillian barre syndrome
Polyneuropathy 1-3 weeks following an illness (70%; respiratory or GI) or vaccination (H1N1, 1976)
An association with preceding Campylobacter jejuni enteritis.
A pt that complains for variable weakness that starts in the legs and ascends leading to paralysis , following an infection or IMR, and has absent DTRs think. ?
Guillian Barre
What are the ADE outcomes of Guillian BArre syndrome
Autonomic dysfunction (loss of vasomotor control): tachycardia, dysrhythmias, hypotension, pulmonary dysfunction, loss of sphincter control, sweating, labile BP
What will the CSF be like in a pt with Guillian barre
High protein with a NML cell count
What is the Tx approach to Guillian barre
IV immunoglobulin Plasmapheresis Hospitalization - ICU admission \+/- intubation Steroids are not helpful
What is the prognosis of Guillian Barre
Self limiting
Patient may need rehab to regain lost function
Minor findings may persist (areflexia)
Fatigue is typical persistent symptom
What is chronic inflammatory demyelination g Poly neuropathy
Occurs in adults M>F
75% have reasonable function after several years following treatment
Death rare
Clinical presentation: -Gradual onset -Initial attack is indistinguishable from GBS -Consider if (chronic course) It lasts longer then 9 weeks Or > then 3 relapses
Sx both motor and sensory.
Symmetric but may be asymmetric in a variant
Considerable variability from case to case
Tremor in 10% of pts
May have cranial nerve findings (external ophthamoplegia)
A pt with external opthomoplegia think..
Chronic inflammatory Demyelinating Poly Neuropathy
A CSF that is acellular with elevated protien… think
Chronic Inflammatory Demyelinating Polyneuropathy
A Electro Dx of Variable degrees of conduction slowing
Prolonged distal latencies
Temporal dispersion of compound action potentials
Conduction block
Evidence of axonal loss is evident in >50% of patients
Think….
Chronic Inflammatory Demyelinating Polyneuropathy
What is the Tx difference of Chronic Inflammatory Demyelinating Polyneuropathy and GBS
Responds to glucocorticoids, whereas GBS does not
What is the Tx approach to Chronic Inflammatory Demylenation Poly Neuropathy
Initiate when progression is rapid or when walking is compromised
If mild, spontaneous recovery can be expected.
Consider IVIg, Plasma Exchange (PE), glucocorticoids
May need to retreat at 6 week intervals
Up to one third fail to respond to initial tx
consider immunosuppressive agents like azathioprine, methotrexate, cyclosporin, and cyclophosphamide
What is Multiple myeloma
Neuropathies with Monoclonal Gammopathy
X-rays will show either lytic or diffuse osteoporotic bone lesions
Effects men more than women
A pt with an elevated ESR in isolation of other systemic disease test.. think
Vasculitic Neuropathy
What is the Tx approach to polyarteritis nodosa
Treat underlying condition causing the vasculitis and aggressive use of glucocorticoids and other immunosuppressive agents
What are the hallmark features of myasthenia gravis
EOMs affected first (diplopia, ptosis)
Dysarthria, dysphagia, and respiratory muscle weakness
Generalized, fluctuating weakness
Symptoms worse towards end of day
Symptoms typically improve with rest and on first arising
If ACh Abs are detected in the blood, think
Myasthenia Gravis
How does myasthenia gravis show on CT
May reveal thymoma: thymic medullary cells can synthesize anti-acetylcholine receptor antibodies
The ice pack test is for what disorder
Myasthenia gravis
What is the tensilon test
Administration of edrophonium 2mg IV
-short acting cholinesterase inhibitor (inhibits ACh breakdown at the NMJ)
Reserved for patients with clinical findings c/w MG and negative antibody and electrodiagnostic test results
Positive test - Definite improvement to weakness
What test can be used for patients with clinical findings c/w MG and negative antibody and electrodiagnostic test results
Tensilon test
What is the Tx approach to Myasthenia Gravis
Anticholinesterase drugs:
-Pyridostigmine 30-60mg 3-4x/day provides symptomatic relief without influencing the course of the disease.
Tailored to the patient’s symptoms
Thymectomy for patients with generalized MG
Cortiosteroids:
-Prednisone can be started at 20 mg orally daily and increased by 10 mg increments weekly to a target of 1 mg/kg/day (maximum daily dose 100 mg).
Plasmapheresis - temporary improvement in rapidly deteriorating cases or to improve condition prior to surgery.
What is myasthenic syndrome
Associated w/ small cell carcinoma
Defective release of acetylcholine in response to a nerve impulse
caused by P/Q-type voltage-gated calcium channel antibodies, and this leads to weakness, especially of the proximal muscles of the limbs.
Unlike myasthenia gravis, however, power steadily increases with sustained contraction
What is the Tx approach to myasthenic syndrome
Prednisone and azathioprine
What are the DDx findings in Myasthenic syndrome vs myasthenia gravis
Unlike myasthenia gravis, however, power steadily increases with sustained contraction in myasthenic syndrome
How does Botulism work
Prevents the release of Ach at NMJ and can cause neuromuscular paralysis
Can be food or wound (rare) borne. Most commonly from home canned foods
What are the S/s of botulism
Weakness begins 12-72 hrs after ingestion (GI)
- Double or blurred vision
- Eye lid lag (ptosis)
- Facial Weakness
- Dysphagia
- Nasal Speech
- Difficulty w/ respirations
- Limb weakness last sign
A child less than one year that presents with constipation, poor feeding, and failur to thrive ( progressive weakness + impaired RR) think?
Botulism
What is the Tx approach to botulism
Initial management – supportive care
Need to be hospitalized and may require ventilator support and aggressive inpatient care
Botulism Antitoxin Heptavalent (equine-derived)
Botulism Immune Globulin Intravenous (human-derived)
-Avoid aminoglycosides and neuromuscular junction blocking medications (potentiate botulism effects)
What medications should be avoided in pts with botulism
Avoid aminoglycosides and neuromuscular junction blocking medications (potentiate botulism effects)
What medications are C/I in myasthenia gravis and lambert Eaton myasthenic syndrome pts
Gentamicin and Strptomycin
What effects go gentamicin and streptomycin have on nerve endings
Prevents the release of ACH from the nerve endings
May be related to Ca++ channel blockade
What is the incubation period for lock jaw
5 days to 12 weeks
Ave 8-12 days
A pt with trismus, dysphagia, facial muscle contortion (risus sardonicus) think
Tetanus: Clostridium tetani
What is opisthotonos
Hyperextended posturing assoc with tetanus
What is the Tx approach to Tetanuc
Human tetanus immune globulin, 500 units, should be administered intramuscularly within the first 24 hours of presentation
General Measures:
Cleaning and Debridement of wound is first step
Tetanus toxoid booster if no vaccination in past 5-10 yrs
Hospitalization in ICU to monitor pulmonary and cardiac function
Metronidazole 500mg IV q6h for 7 days (preferred abx)
Heavy sedation with benzodiazepines for muscle spasms
Mortality 10-60% (95% who recover do so without long-term sequelae)
Decreased through early detection
What is the perferred ABX in tetanus
Metronidazole
What is pyridostigmine bromide
Nerve agent pretreatment
Increases the amount of nerve agent a person can be exposed to and survive
What is the Tx approach to nerve agents
Emergency measures Supportive measures Meds: -Atropine 2mg -2Pam Cl
What is pralidoxime
Protects acetylcholinesterase from degredation
Irreversible binding by nerve agent
AKA: 2 PAM Chloride
Spasticity implies that the lesion originates
UMN
Rigidity implies
Extrapyramidal dysfunction
Hypotonia implies
LMN lesion or myopathy
A pt w/ Spasticity, diffuse weakness, hyperreflexia, positive Babinski; no muscle atrophy until late where is the lesion
UMN
A pt w/ Flaccidity, focal weakness, hyporeflexia, negative Babinski, wasting of muscles where is the lesion
LMN
Hyper reflex ismplies what lesion
UMN lesion
Hypo reflexia implies what lesion
LMN
When reflexes are asymmetric and lateralized its typically a lesion where?
UMN on the brisk side
A focal deficit implies
A rott/ plexus/ peripheral nerve lesion
A pt with loss of distal DTRs yet proximal DTRs remain intact, suspect
DM poly neuropathies
What are the 5 types of imbalance
Imbalance with Cerebellar ataxia
Cerebellar limb ataxia
Imbalance with vestibular dysfunction
Imbalance with sensory ataxia
Sensory limb ataxia
Where is the lesion in Hemiparetic gait
UMN caused by Brain stem, Cerebral hemisphereStroke, tumor, trauma
The upper extremity adducted and internally rotated
Flexion at elbows, wrist and fingers
Extension at hip, knee and ankle
Forward swing of the spastic leg requires abduction and circumduction
Contralateral tilt of the hip to help with swing phase
The patient will have to “circumduct” or swing the leg around to step forward.
A scissor gait is AKA? And is common in what pts
Paraparetic or Diplegic gait
And common from stroke
Often from periventricular lesions
The patient has spasticity in the lower extremities greater than the upper extremities.
Hips and knees are flexed and adducted with the ankles extended and internally rotated
The patient circumducts the lower extremities
Upper extremities are held in a mid or low guard position.
Often seen with periventricular lesions.
The legs are more affected than the arms b/c the corticospinal tract axons that are going to the legs are closest to the ventricles.
What is a steppage or neuropathic gait associated with
Usu. assoc. with L5 lesion if unilateral, however if bilateral consider polyneuropathy or lumbosacral poly radiculopathy
Most often seen in peripheral nerve disease
The distal lower extremity is most affected.
Causes weakness of the foot dorsiflexors
B/C they are weak the pt will have a high stepping gait
This is an attempt to avoid dragging the toe on the ground
Causes: sensory neuropathy; vitamin B12, tabes dorsalis
A waddling or myopathic gait is caused by,..
Caused by myopathy, NMJ disease, or proximal symmetric spinal muscular weakness
The proximal limb weakness. With weakness of hip flexion the trunk is tilted away from the leg that is being moved
This provides additional distance between the leg and the floor
The pelvis is rotated to forward to assist in forward motion
The patient will not be able to stabilize the pelvis as they lift their leg to step forward
The weakness is normally bilateral causing the typical waddling type gait
Describe a parkinsonian gait
Forward stoop, modest flexion of hip and knees.
Arms flexed at elbows and adducted at shoulders
4- to 6-Hz resting pill-rolling tremor in his hands.
Bradykinetic gait initiated by a slow lean forward and maintained small, shuffling steps
Gait tends to accelerate
Falls are common due to postural instability and freezing of the gait
Turns en bloc (all together, or as a whole) like a statue
There is decreased facial expression
Describe apraxia
Found in bilateral frontal lobe disease.
May be accompanied by dementia and incontinence
Caused by an inability to plan and execute sequential movements
Resembles the Parkinsonian gait
-Stoop posture with short shuffling steps
Difference in initiation though
-When patient is asked to step forward while standing, there is a long pause before any attempt is made to flex at the hip and knees
Once started the gait is only maintained for a few steps then patient has to stop for several seconds or longer
A gait with a lurching appearance, unpredictable movements, and Intrusion of intermittent, irregular, jerky, involuntary movements in both the upper and lower extremities
Choreoathetotic gait
Basal ganglia D/o
A gait that is wide based, with truncal instability w/ erect posture, and
Irregular lurching steps in which speed and stride vary
Results in lateral veering and if severe, falling.
Cerebellar ataxia gait!
Assoc. with Cerebellar disease.If there is disease of the cerebellar hemispheres, limb ataxia and nystagmus is often present
A pt that resembles a cerebellar gait, board stanced with difficulty changing positions yet can maintain balance with eyes open, but falls in the Romberg test has what gait
Sensory Ataxia
A pt with asymmetric nystagmus, normal proprioception, and normal strength, and tend to fall to one side.. has what type of ataxia
Vestibular
Describe a stasis-abasia
A psychogenic gait disorder
Physical Exam shows normal coordination of leg movement while lying or sitting
Yet patient is unable to stand or walk without assistance
But if distracted they can maintain balance and may be able to take several steps
But this is usually followed by a dramatic demonstration of imbalance with lunge toward support
What are the 4 characterizations of MS
Inflammation
Demyelination
Gliosis formation
Neuronal loss
What is the age of onset fo MS
20- 40 years old typically women of European lineage
What are the 4 major RSK fxs for MS
genetic predisposition
Vitamin D deficiency
Epstein-Barr virus (EBV) exposure after early childhood
Cigarette smoking
20-40 year old woman that presents with sensory loss, optic neuritis, and weakness think
MS
What is Inter nuclear opthalmoplegia
Impaired adduction of eye 2ndary to lesion in ipsilateral medial longitudinal fasciculus often seen in MS pts
What Nerve palsy is common in MS
CN 6 palsy
How can you tell the difference between MS and Bell’s palsy
Unlike Bell’s palsy, MS not associated w/ ipsilaeral loss of taste or retroauricular pain
What are the 3 clinical types of MS
Relapsing-Remitting Dz
-Most common (90% of cases)
Secondary progressive Dz
-Always begins as RMS then has steady deterioration
Primary Progressive Dz
-Steady progression from onset
What is the D criteria for MS
Requires evidence that at least two different regions of central white matter are affected at different times.
Bright lesions in the white matter of the cerebral hemispheres, brain stem, and spinal cord
Contrast (ie gadolinium) enhances the lesions
What is the hallmark of Dx for MS
Two or more episodes of symptoms and Two or more signs (weakness, fatigue, sensory loss, motor loss, blindness)
Symptoms longer than 24hrs
Involvement of anatomically white matter tracts of the CNS.
Distinct episodes separated by a month or more.
How will CSF present with MS
oligoclonal banding in the cerebrospinal fluid.
What is the Tx approach for acute flare ups of MS
Managed with glucocorticoids
- Methyprednisolone 1g daily IV for 3 days
- Then oral prednisone 60-80mg/day x 1 wk then tapered
What is the Tx approach for long tern immuno modulation for RMS
Beta-interferon ie Avonex 30mcg IM q week
Glatiramer acetate 20mg SQ daily
What is the DOC from Primary progressive MS
Ocrelizumab
What are three things that can lead to thinking MS will have a favorable prognosis
Optic neuritis or sensory symptoms at onset
<2 relapses in first year
Minimal impairment after 5 years
What is the RSK of developing MS if the MRI shows three or more typical T2 weight lesions
80 percent at 20 years
A pt presents with MS symptoms ( optic neuritis) and behavioral changes and cognitive abnormalities thing..
ADEM
Acute Disseminated Encephalomyelitis
What is the hallmark of ADEM
Hallmark is the presence of widely scattered small foci of perivenular inflammation and demyelination as compared to MS which has large confluent demyelinating lesions.
How does the CSF of ADEM present
Lymphocytic pleocytosis
Elevated protein
Oligoclonal bands are rarely seen (unlike MS)
What is the Tx approach to ADEM
Recovery is typically complete
IV corticosteroids often shorten the course and lessens the
severity
What is the most common progressive motor neuron Dz
ALS
What are the S/s of ALS
Sx:
Example: LMN – asymmetric weakness
W/ sensory, bowel/bladder, cognition
intact
Dx:
Simultaneous UMN & LMN involvement
w/ progressive weakness
What is the Tx approach to MS
No Cure
Riluzole, 50mg bid po
-Increased short-term survival
Edaravone 60mg IV
-Slows dz progression in pts w/ mild dz
symptomatic Tx
How is polio spread
Fecal oral
Enterovirus
What part of the spine does polio effect
Anterior horn cells
How is polio Dx
Stool or NP secretions
Lesions at T6 result in loss of what reflexes
Abdominal reflexes
What type of dysfunction results from lesions above the sacral level
Bowel and bladder dysfunction
Lesions at the right dorsal column at L1 produce what impairment
Ipsilateral loss of vibration/position sense generalized below the lesion level
What is a common cause of dorsal column lesions at L1
Common causes include MS, penetrating injuries, and compression from tumors.
Lesion of the right fasciculus cuneatus at C3 produces what impairment?
Ipsilateral loss of vibration and position in the right arm and upper trunk.
What are common causes of Right fasciculus cuneatus lesions at C3
Common causes include MS, penetrating injuries, and compression from tumors.
Lesion of the right lateral corticospinal tract at L1 produces what impairment?
Ipsilateral upper motor neurons signs generalized below the lesion level -UMN signs Weakness (Spastic paralysis) hyper reflexia (+ Babinski, clonus) Hypertonia
What are common causes of lateral corticospinal tract lesions
Common causes include penetrating injuries, lateral compression from tumors, and MS.
lesions of the elateral spinothalamic tract produces what impairment
Contralateral loss of pain and temperature sense
What are common causes of lateral spinothalamic tract lesions
Common causes include MS, penetrating injuries, and compression from tumors.
Lesion of the anterior gray and white commissures (Central Cord Syndrome) at C5-C6 produces what impairment?
Blanket or cape dermatomes pattern
Impaired pain and temperature
sensation, C5-C6 dermatomes,
bilaterally
What is a common cause of central cord lesions
Common causes include posttraumatic contusion, syringomyelia, and intrinsic spinal cord tumors.
Complete transection of the spinal cord (Transverse Cord Lesion) at L1 would produce what impairments?
Bilateral loss of vibration and position sense
( dorsal column lesion)
Bilateral UMN signs
(Lateral corticospinal tracts lesion)
Bilateral Loss of pain and temp sense
(Lateral spinothalamic tract)
Complete transection of the dorsal columns, bilaterally, (Posterior Cord Syndrome) in the cervical region would produce what impairments?
Bilateral loss vibration and position sense, generalized below lesion level
Complete transection of the lateral corticospinal and lateral spinothalamic tracts with sparing of the dorsal columns, bilaterally, (Anterior Cord Syndrome) in the cervical region would produce what impairments?
ipsilateral UMN signs
( lateral corticospinal tract lesion)
And Contralateral loss of pain and temp sense
( lateral spinothalamic tract lesion)
What are the two types of cord compression tumors
Intramedullary – 10%, Ependymomas most common type, Gliomas make up the rest
Extramedullary – 90%, most commonly related to Neurofibromas and Meningiomas.
What is the most common Extrapyramydal type of cord tumors
Extrapyramidal
-neurofibromas and mengiofibromas
How will the CSF present with spinal tumors
Xanthochromatic
Greatly elevated protein
Normal or elevated WBC
Normal or depressed glucose elevation
Quenckenstedt Test may reveal a partial or complete block
Where are the most common locations for disc prolapse
L4-5 and L5-S1
A pt presents with specific radicular pain, abnormal posture, and Limited ROM.. suspect
Disc prolapse
Loss of DTRE is more suggestive of a root lesion
What are the 4 criteria for referral to spine ortho or MRI in Disc prolapse
Progressive motor weakness from nerve root injury
Bowel/bladder disturbance or other sign of cord compression (cauda equina)
Incapacitating pain for at least 4 weeks
Recurrent incapacitating pain despite conservative treatment
How does Neurogenic Shock present
Loss of sympathetic tone
Reduced systemic vascular resistance
Hypotension
No Tachycardia!
A lesion at the optic chains presents with what blindness
Loss of lateral visual fields
Describe the pupillary pathway
Light impulse travels up optic nerve, divides at the chiasm, arrives at pretectal nucleus. (Afferent)
Efferent signals sent via CN III to cause direct and consensual constriction
Temporary decrease of blow flow to the retina presents as
Transient monocular blindness
(Vision loss in one eye, CNII deficit)
Aka: Amaurosis Fugax
What is most common cause of Inflamation to the optic nerve
MS
A pt with subacute unilateral vision loss, that develops over a few days and has low serum vitamin D,… think
Optic neuritis associated with MS
Pallor of the optic disk is a sign of
Late finding in optic neuritis from MS
What is the Tx approach to Optic neuritis
IV methylprednisolone 1 g daily for 3 days followed by a tapering course of po prednisolone
What is the prognosis of Optic neuritis
Associated with a 50 percent progression of MS
( optic neuritis and pain with EOM is an early sign of MS)
What is giant cell arthritis/ temporal arteritis
Inflammation of the external carotid artery at the superficial temporal artery that may lead to blindness
A pt with Jaw Claudication, headache, scalp/ temporal tenderness, Visual S/s and throat pain… think
Giant cell arteritis
What is the Tx approach to Giant Cell Arteritis
Prednisone 60 mg PO daily
In order to start Tx for Giant cell arteritis what must be done (according to current)
Artery Bx
However the teacher says just start on prednisone
Marcus Gunn/ swinging light test assess for
associated with disease of retina or optic nerve
Sensory system deficit
What is papilledema a sign of
ICP ( search for the cause)
What is the cardinal S/s of papiledema
HA esp. when recumbent
What CN palsy is apparent in papilledema
CN VI palsy
A pt with a “down and out” fixed gaze, +diplopia, + ptosis .. think
CN III palsy
New onset CN III palsy with pupillary involved.. order
MRI/ MRA r/o cerebral artery aneurysm
Interruption of the cervical sympathetic nerves to the eyes leads to…
Ptosis, miosis, and anhidrosis
Horner syndrome
What should be r/o in Horner syndrome
Lung tumor or Carotid Artery Aneurysm
A pt with ptosis of the eyelid on the side of the small pupil =>
Horners syndrome
A pt with ptosis of the eyelid on the side of the large pupil =>
the patient has a partial third nerve lesion on that side
CN III palsy
Argyll Robertsons pupil aka prostitutes pupil presents
Pupil does accommodate to near vision
Pupil does not react to light, either directly or consensually
Associated with CNS syphilis and other conditions
A tonic pupil with parasympathetic denervation that constricts poorly to light but reacts better to accommodation
Adies pupil
Benign
How does CN IV palsy present
Up and In deviation of the eye
What is the most common cause of CN IV palsy
Head trauma
What should be evaluated If a pt has CN VI palsy what should be evaluated
MRI! ICP UPO
A pt with an adducted eye at rest that can not abduct the eye has what CN palsy
VI
CN V present how
AKA Tic douloureux
Lancinating pain in distribution of one or more branches of CN V – lower 2/3 of face.
10/10 pain along the lower 2/3rd of the face is a sign of
CN V palsy
What is the Tx approach to Trigenminal neuralgia ( CN V)
Spontaneous recovery
Treatment options include
-Carbamazepine
Can cause agranulocytosis
Monitor w/ CBC and LFTs
-Oxcarbazepine
Less bone marrow toxicity than carbamazepine
CN VII is called what
Bell’s palsy, LMN problem
What is the most common form of facial paralysis
Bell’s palsy ( CNVII)
Pain behind ear followed by facial paralysis with an assoc loss of taste is what
Bells Palsy ( CN VII LMN)
A pt with Bell’s palsy, yet the forehead lesions are intact think..
Central lesion
What is the Tx approach to Bell’s palsy
Prednisone 60 mg x 5 days, then tapered 5 days
Herpes Zoster along CN VII is called what
Ramsay Hunt Syndrome
Presents with Facial weakness
( like Bell’s palsy)
Vesicular rash, vesicles on the tympanic membrane
Assoc with decrease hearing
What is the Tx approach to Ramsay Hunt Syndrome
Acyclovir and Famiciclovir with steroids
A Weber test that laterlized to one side and the BC is greater than AC conduction on the same side is what kind of hearing loss
Conductive
A Weber test that lateralizase away from the lesion and the AC > BC on the side of the lesion is what kind of hearing loss
Sensorineural hearing loss
What is the most common cause of CN VIII dysfunction from a tumor
A Schwannoma or meningioma
A d/o in the gene tranrythrein is what d/o
Familial amyloid
