Upgrade to remove ads
Robbins Neuro block 2
Terms in this set (38)
1: Amyotrophy -
2: Muscular Dystrophy -
3: Myalgia -
4: Myoglobinuria -
5: Myokymia -
1: Amyotrophy - Muscular atrophy from axonal loss from the anterior horn cells.
2: Muscular Dystrophy - is any condition due to genetic abnormal muscle development, often denoting the degeneration of muscles.
3: Myalgia - pain from any muscle disease or disorder
4: Myoglobinuria - the presence of myoglobin in the urine usually associated with rhabdomyolysis or muscle destruction.
Crush injury, vascular problems, venoms, certain drugs (statins) can damage the muscle, releasing myoglobin into the circulation and thus to the kidneys.
Too much myoglobin released into the circulation can occlude the renal filtration system leading to acute tubular necrosis and acute renal insufficiency.
5: Myokymia - persistent quivering of a muscle
6: Myopathy -
7: Myositis -
8: Myotonia -
9: Polymyositis -
10: Rhabdomyolysis -
6: Myopathy - any muscle disease either acquired or hereditary.
7: Myositis - Any inflammation of the muscle. For example, sore muscles after weight lifting.
8: Myotonia - prolonged muscle contraction after voluntary contraction or percussion, which can be tested by hand grip, forced eye closure, or muscle percussion.
Refers to a delay in muscle relaxation demonstrated after voluntary action (such as hand grip or forced eye closure) or percussion of a muscle such as the thenar or wrist extensor muscles (percussion myotonia)
Results from several different abnormalities of muscle membrane and is treated with membrane-stabilizing drugs (quinine, procainamide, and phenytoin).
Seen in various Disorders.
9: Polymyositis is a chronic inflammatory myopathy.
10: Rhabdomyolysis - a condition in which damaged skeletal muscle tissue breaks down rapidly; its complications are significant problems for those injured in disasters such as earthquakes and bombings.
Routine labs for possible muscle damage:
Creatine phosphokinase (CPK) level ---------
Electrolytes, calcium, magnesium
Serum creatinine and BUN
Urinalysis: Myoglobinuria is indicated by + urinalysis with few
RBCs on microscopic exam.
Thyroid Function Tests
Sedimentation rate (Sed Rate) & C Reactive Protein (CRP)------------Its an 'itis' if sed rate and CRP are off------
Name the five most common muscular dystrophy types:
1: Duchenne MD (dystrophin defect)-------children, devastating, no dystrophin
2: Becker's MD (dystrophin defect)---------adult appearance, milder, some dystrophin -----pseudohypertrophy (fat replacement)
3: Facioscapulohumeral dystrophy (Deletion of D4Z4 repeats and a "toxic gain of function of the DUX4 gene)
4: Limb-girdle dystrophy (defects in proteins that make up the dystrophin-glycoprotein complex)
5: Myotonic dystrophy (expansion of a short repeat in the DNA sequence (CTG in one gene or CCTG in another gene).
Basics of Duchenne's Muscular Dystrophy:
-males only (X-chromosome, region p21)
-initially some muscle weakness (development reverts)
-DTRs normal but diminish with age
-Gower's sign, "toe-stand"
-wheelchair by age 10 yrs
-death around 20 yrs
Lab results for Duchenne's dystrophy?
DMD typical labs:
1: Elevated Creatine Phosphokinase (CPK) - 15,000 to 20,000 U/L. (highest of all the dystrophies). Normal values of CPK is <195 U/L.
*Elevated CPK levels are found in 50 to 70% of the female carriers.
2: EKG abnormalities are present in 80% (true cardiomyopathy is rare).
3: Needle EMG shows myopathic changes (more on this later).
4: Blood tests show the gene for the protein dystrophin to be absent or abnormal.
5: Muscle biopsy reveals fiber destruction with marked fibrosis and shows extremely low levels of dystrophin in the muscle.
Basics of Becker's Dystrophy:
Same genetics as Duchenne's (x-chromosome, region p21)
Dystrophin my be present but altered, or in very low amount.
Later onset (5-15 yrs)
Longer lifespan (40-50 yrs)
Less intellectual impairment
1: Serum CPK is moderately elevated 20 to 80 times normal (not as high as DMD).
2: ECG is abnormal in 30% to 40%.
3: Muscle biopsy reveals findings similar to, but less severe than, DMD.
4: EMG is myopathic.
**60% of female carriers have elevated CPK
Explain basics of FSHD:
-weakness of face, scapular muscles
--------frequent winged scapula, (true)hypertrophic deltoids
--------Sensorineural hearing loss (especially with younger age of onset).
--------Reflexes only impaired at biceps and triceps.
Diagnosis for FSHD:
(deletion on chromosome 4q35)
-serum CK elevated in 75% of cases
-muscle biopsy pathognomonic
Basics for Limb-Girdle dystrophy:
Male=Female (autosomal dominant or recessive)
Wasting pattern shown
1: Serum CPK - up to 10 times normal.
2: EMG - nonspecific myopathic changes.
3: Muscle biopsy - nonspecific dystrophic changes.
Basics of myotonic dystrophy:
Most common dystrophy
onset: any age, usually 20-30 yrs
multi system involvement--
--CARDIAC ABNORMALITIES PROMINENT
--Loss of facial expression and ptosis marked wasting of masseters and temporalis giving a haggard, wasted appearance to the face.
--Cataracts in 90% of patients.
--Dysarthria due to myotonia of the tongue.
--Dysphagia due to esophageal myotonia.
--Wasting of the sternocleidomastoids early feature and patients may have difficulty in lifting the head from a pillow. The neck is thinned producing a "swan neck".
--Many have a low I.Q. and dementia may occur
--Endocrine dysfunction (Gynecomastia, gonadal atrophy, and insulin resistance).
--Gut motility low
--Frequent respiratory infections: muscular difficulties and Ig abnormal.
Myotonic dystrophy dx:
Myotonic dystrophy dx:
1: EMG study: characteristic a "Dive Bomber"
2: CPK is normal or mildly elevated.
3: Muscle biopsy: DNA testing for CTG expansion.
*may require pacemaker
*Quinine, procainamide, phenytoin-- to reduce myotonia
Describe McArdle's disease:
Metabolic disorder- glycogen storage
Chromosome 11q13 (glycogen phosphorylase)
Onset in first 10 yrs
-Cramps, myoglobinuria, rhabdomyolysis
-SECOND WIND-after short period
CPK almost always elevated
----forearm ischemic test------ammonia does NOT increase
--high carb diet recommended
Basics of channelopathies (periodic paralysis)
All autosomal dominant
1: Hyperkalemic periodic paralysis - K⁺ leaks out of cells
2: Hypokalemic periodic paralysis - K⁺ leaks INTO cells
3: Myotonia congenita - episodes onset with COLD temps
4: Malignant Hyperthermia - triggered by drug exposure
--hyperkalemia, hyperthermia, myoglobinuria
Basics of Myotonia Congenita:
Male = female
*Reactive to Exercise*
1: Myotonia at birth
2: Peculiar cry
3: Difficulty feeding
4: Inability to re-open eyes while having face washed
Life expectancy normal
1: possibly autoimmune
2: Subacute onset of progressive proximal muscle weakness (not muscle pain/minimal muscle tenderness)
3: Skin involvement (dermatomyositis)
4: Serum muscle enzymes ( CPK and aldolase) elevated
(Heliotrope rash shown)
Gorton's papules also possible (knuckles)
Explain Inclusion Body Myositis:
It is the most common acquired inflammatory muscle disorder seen in people over 50.
*IBM is often initially misdiagnosed as polymyositis.
Get a biopsy
Weakness develops long term
Patients may become unable to perform daily living activities and most require assistive devices within 5 to 10 years of symptom onset.
A course of prednisone is typically completed with no improvement
Explain Volkmann's ischemic contracture
Swelling of injured arm----ischemic muscle death in arm
Prevent compartment syndrome by surgical release
Explain Transient neonatal myasthenia gravis
--Infant receives anti-ACh-R enzymes from mother
--should recover in a week after birth
Compare eye reactions for:
M.G. - Ptosis, Pupil intact,
B. - Dilated pupils, poor reaction
L.E.S. - Extraocular muscles intact
Leaves Eyes alone
A 64-year-old woman presented with a 1-year history of progressive fatigue, particularly trouble walking up and down stairs and difficulty arising from a chair. Lately she had noted slightly slurred speech, transient horizontal diplopia with ptosis, dry mouth, and tingling in the feet and legs. She had a 80-pack-year history (2 pk/day/40yr) of cigarette smoking.
Examination abnormalities included mild weakness of orbicularis oculi, neck flexors, deltoids, triceps, and iliopsoas muscles with difficulty arising from a chair. Her speech was slightly dysarthric. Muscle stretch reflexes were absent but displayed post exercise enhancement.
Lambert-Eaton Myasthenic Syndrome (LEMS) a presynaptic neuromuscular transmission disorder. Serum voltage-gated calcium channel (VGCC) antibodies were increased. A chest radiograph showed a right hilar mass; its biopsy revealed small cell lung cancer (SCLC). The patient received chemotherapy and 3, 4-diaminopyridine for symptomatic treatment of LEMS, resulting in some improvement in strength. She died 16 months later from small cell cancer.
A period of several weeks, blurred vision and "droopy eyes"
developed in a previously healthy 38-year-old woman. Her
symptoms worsened toward the end of each day and often
cleared overnight. Friends commented that her speech had
become more difficult to understand and softer in volume. She
also described increased tiredness on climbing stairs;
sometimes she had to stop and rest while cleaning her teeth or
brushing her hair.
Neurologic examination revealed bilateral ptosis and
disconjugate eye movements in several directions of gaze.
There was weakness of eye closure and neck flexion and
mild proximal limb weakness
An edrophonium (Tensilon) test resulted in marked improvement for 3 to 4 minutes. Repetitive motor nerve stimulation testing demonstrated a 15% decrease in the ulnar compound muscle action potential amplitude between the first and fifth stimuli. Anti-acetylcholine receptor (AChR) antibodies were present in significantly abnormal titers confirming Myasthenia Gravis. Results of CT scanning of the mediastinum were unremarkable. Immunosuppressive and pyridostigmine bromide (Mestinon) treatments were initiated, with plans for the patient to undergo thymectomy when her symptoms were under control
A 7-year-old boy presented with recurrent episodes of generalized weakness, usually after hockey games. Each event resolved within 30 minutes after onset, without associated respiratory distress, dysarthria, or dysphagia. At his worst, the boy could not stand or raise his hands over his head. During the winter months, he noted stiffness in his hands and found it difficult to open his eyes quickly after blinking. His mother recalled having similar episodes but none since late adolescence.
Physical examination results were normal.
Follow up: His symptoms were controlled by carbohydrate loading before increased activity
---hyperkalemic periodic paralysis---
Myotonia is a nonspecific finding
symptoms were episodic
*Carb-loading is the key here.
-Carbs increase insulin levels
-Insulin increases K⁺ influx into cells
-If successful, it was hyperkalemic periodic paralysis
During another episode, the patient had an increased serum potassium level of 6.4 mmol/L, confirming the diagnosis of hyperkalemic periodic paralysis.
A 17-year-old boy presented with severe pain, stiffness, and "hardening" of his forearm muscles while moving the contents of his friend's house. In the immediate aftermath, he noticed that his urine was "Coca-Cola" colored.
Hours later, his physical examination results were normal with the exception of the muscle tenderness to palpation. His serum creatine kinase (CPK) level was increased 50 times normal. His BUN was increased, and myoglobin was in his urine. The patient was admitted to the hospital and treated with vigorous IV hydration.
His symptoms resolved within several days.
A forearm exercise test demonstrated the expected increase in venous ammonia levels without the expected increase in lactate.
Myopathy Presenting with Exercise Intolerance.
Muscle biopsy revealed subsarcolemmal blebs seen on a periodic acid-Schiff-stained muscle biopsy specimen which are consistent with glycogen excess.
-decreased myophosphorylase = diagnosis of McArdle disease.
A 14-year-old boy presents for examination because his friends tease him about the way his shoulders "stuck out in the back." Further questioning reveals that for the past year, he has noted weakness in his arms and legs, which worsened to the point that he was forced to drop out of the swim team. His uncle had died at an early age from a muscular disease.
Examination revealed tapir lips (pouting), pole neck, symmetric weakness, and atrophy of the muscles of the shoulder girdle, hips, and thighs. A muscle biopsy confirmed the diagnosis.
Muscular dystrophy is an uncommon hereditary disorder of childhood and early adolescence. It presents in a variety of ways, most commonly as Duchenne's muscular dystrophy, myotonic dystrophy, or facioscapulohumeral dystrophy, as in the case presented here. The course usually is progressively downhill, with death due to respiratory failure in the second to fifth decade. Diagnostic workup should include routine CBC, urinalysis, and chemistry panel; a thyroid profile to exclude hypothyroidism; EMG; and muscle biopsy. The CPK is elevated in most cases.
A 40-year-old man presents with weakness of all four extremities, facial weakness, and dysarthria of several months' duration.
Neurologic examination revealed bilateral ptosis; a "hatchet face," depicting the facial weakness; weakness on flexion and extension of the hands, fingers, feet, and toes; distal atrophy of the muscles of the extremities; slow relaxation of the hand grip; and myotonia of the thenar eminence and tongue. In addition the patient demonstrated premature baldness, cataracts, and testicular atrophy. The diagnosis was confirmed by EMG and muscle biopsy.
The myotonia gives it away.
A 35-year-old woman with genetically proven myotonic dystrophy presents to your clinic. Her chief complaint is fatigue. She has not seen a physician in several years. She complains of bilateral foot drop and distal hand stiffness but denies any other problems. Social History: She does not smoke or drink. She finished high school at 19 and took one semester of college work. She is recently married. In her family history, she reports that her father wears braces and uses CPAP at night.
You recommend for the patient:
A: No need to worry, that everything appears fine.
Many myotonics are fatigued and she should "take it slow".
B: Baseline EKG, overnight polysomnography, and genetic counseling.
C: MRI of the brain, EEG, and respiratory therapy.
D: As a patient with myotonic dystrophy, she has decreased mental capacity and should appoint a power of attorney.
C. Cardiac abnormalities in myotonic dystrophy are common and should never be overlooked
A 32-year-old woman is seen in the neurology outpatient clinic with symptoms of diplopia and ptosis that fluctuate during the course of the day.
Examination shows the ptosis increases with sustained upward gaze. Routine laboratory studies were normal.
Which of the following statements concerning the above case is true?
A: It is an autoimmune disorder caused by antibodies that are directed against presynaptic nicotinic acetylcholine receptors.
B: It is an autoimmune disorder caused by antibodies directed against postsynaptic muscarinic acetylcholine receptors.
C: It is an autoimmune disorder caused by antibodies directed against presynaptic voltage-gated calcium channels.
D: It is an autoimmune disorder caused by antibodies directed against postsynaptic nicotinic acetylcholine receptors.
E: It is an autoimmune disorder caused by antibodies directed against the synaptic enzyme acetylcholinesterase.
-Ptosis is key
D. The primary antigenic target in autoimmune myasthenia gravis is the post synaptic nicotinic acetylcholine receptor. Presynaptic voltage-gated calcium channels are the target of the Lambert-Eaton myasthenic syndrome.
A 40-year-old female is seen by you complaining of a 3 month progressive muscle fatigue with climbing stairs and carrying objects. The patient noted a rash on her cheeks, neck, chest and her hands and swelling around her eyes. Review of systems revealed: sensitivity of her fingers to cold temperatures, difficulty swallowing certain foods, and some shortness of breath on exertion.
Neurologic examination reveals proximal muscle weakness in the arms and legs. Reflexes, and sensation are normal. Laboratory studies are normal except for elevated CPK of 770 mg/dl.
Dermatomyositis (DM) is characterized by painful proximal muscle weakness (as is polymyositis). DM is distinguished from polymyositis by the associated heliotrope (purplish discoloration of the eyelids) and Gottron patches (papular erythematous scaly lesions over the knuckles). DM may occur in the context of systemic sclerosis or other mixed connective tissue disease, and there is an increased incidence of malignancy in patients with DM. Polymyositis is more often associated with other autoimmune diseases, including Crohn's disease, vasculitis, sarcoidosis, and Myasthenia gravis. Corticosteroids are the mainstay of treatment in polymyositis and DM.
Sarah, a twenty-one year old student at Iowa State University had spent Thanksgiving day with relatives at her grandparent's farm. During her drive back to campus on Friday morning her vision became blurry, and she was forced to pull over to the side of the road. As she sat in her car, her vision worsened. She opened the car hood in hope of attracting aid and tried to relax. In a short time, a highway patrol officer pulled over and approached Sarah. By this time, Sarah was having trouble swallowing and speaking clearly. The officer helped Sarah to his car and rushed her to the emergency room at a nearby hospital.
In the ER, Sarah was able to describe her symptoms to a physician. The physician made note of what Sarah had eaten during the last 24 hours and was especially interested in the fact that Sarah's grandmother canned all of her own vegetables.
Why no antibiotics?
Treatment with antibiotics would release more toxin in the blood stream and could be potentially fatal.The physician observed that Sarah's breathing was becoming labored. She ordered Sarah's blood sampled, her gastrointestinal tract pumped, and a mechanical respirator prepared for use. Fearing that Sarah suffered from a case of botulism, she asked that Sarah's grandparents be contacted and samples of the Thanksgiving meal retained, if possible, and sent to a local clinic for analysis.
A 54-year-old football coach was evaluated for right foot drop first noted 6 weeks earlier when he tripped over his right foot. Tripping subsequently occurred with increasing frequency, especially when walking on uneven surfaces. He had no recent trauma or illness and no back, buttock, or radicular leg pain. Numbness developed over the lateral lower leg and dorsum of his foot. His medical history was unremarkable; there was no personal or family history of diabetes or nerve palsy.
Examination revealed a healthy man with normal appearing lower extremities. However, he reported tenderness to palpation at the proximal lateral knee where there was an associated fullness without a discrete mass. Pain was not reproduced with various joint manipulations, all of which were normal. Motor examination disclosed weakness in right toe extension, foot dorsiflexion, and eversion. Plantar flexion and inversion of his right foot, knee flexion, and hip abduction were totally preserved. Sensation was diminished to pinprick and monofilament touch on the dorsum and first web space of the right foot. He had normal muscle stretch reflexes.
What does he have and where is the cause located?
-Superficial peroneal neuropathy - compression at fibular head
-Deep peroneal neuropathy - compression at fibular head
-Common peroneal neuropathy - compression in the popliteal fossa
-Sciatic neuropathy - compression in the mid thigh
-Tibia neuropathy - compression in the distal thigh
Answer: C: EMG defined a predominately axonal, common peroneal neuropathy, with sparing of the short head of the biceps femoris. Because of the progressive course, the local fullness and discomfort. MRI of the popliteal fossa was performed, demonstrating a large ganglion cyst emanating from the proximal tibiofibular joint. Surgical excision of the cyst with decompression of the common peroneal nerve at the proximal tibiofibular joint led to complete recovery of motor function within 3 months.
A 50-year-old woman, an avid gardener, presented with a 2-year history of her right hand "falling asleep." Initially, this occurred only in the morning on awakening. Three months before evaluation, these symptoms began to awaken her at night and were also noted while driving a car or blow-drying her hair. She reported that "all" her digits were affected and that her Paresthesias were sometimes accompanied by aching of the wrist and forearm. She did not report problems with hand strength. More recently, she was experiencing similar but milder symptomatology in her left hand.
Neurologic examination disclosed minimal weakness of right thumb abduction, without loss of thenar eminence bulk. Results of reflex and sensory examinations were normal, including 2-point discrimination and graded monofilament touch. What would you expect to find on the examination of her right upper extremity and what is the diagnosis?
-turn for questions--
--What is her clinical diagnosis?
Carpal Tunnel Syndrome
Cubital Tunnel syndrome
Anterior interosseous syndrome
Posterior interosseous syndrome
--Select the most characteristic clinical feature for diagnosis in the above condition.
Occurs with greater frequency in men and in the dominant hand
Sensory symptoms can be mimicked by the neurogenic thoracic syndrome
A Tinel's sign has a high specificity as a clinical feature in this condition
An early symptom of this condition is asymmetric nocturnal hand paresthesias
A similar pattern of hand weakness can be seen in a C6-C7 radiculopathy
2) D: Her symptoms were reproduced by foraminal compression maneuvers, such as nerve percussion (Tinel sign) over the median nerve at the wrist.
A 21-year-old-male student presents with numbness and tingling over the 4th and 5th digits of his right hand. States he notices it when he studies and he has to move his hand and the symptoms improve. He has no weakness at this time but you notice slightly diminished pinprick of the entire 5th digit and ulnar half of his 4th digit of his right hand.
Which of the following is the most common location causing his problem?
C, This is cubital tunnel syndrome with compression of the ulnar nerve at the elbow.
Following a bout of alcoholic intoxication, a 25-year-old man developed weakness of the right wrist and finger extension and right brachioradialis, with preservation of triceps and deltoid function.
--Which of the following is the most likely diagnosis?
Posterior interosseous syndrome
Radial neuropathy at the spiral groove
Posterior cord brachial plexopathy
Radial sensory neuropathy
--Another condition that may present with similar symptoms
Ischemic damage to nerves in forearm
Anterior interosseous syndrome
1) B, Saturday night palsy.
2) B, Lead loves the radial nerve
A 45-year-old overweight bartender was evaluated for sensory complaints of 4 months' duration of her left thigh. She described an aching discomfort extending down the lateral aspect of her thigh, intensified by standing or walking. She also described a burning numbness in the area where her hand would rest if put in her front pants pocket. There was associated cutaneous hypersensitivity with an aversion to having clothes or bed sheets rub against her. She was unaware of any other precipitating events.
Examination demonstrated an elliptically shaped area of sensory loss on the distal half of her anterolateral thigh. She had no atrophy, weakness, or reflex loss.
--Your diagnosis is?
C: This is typical of Meralgia Paresthetica due to compression of the lateral femoral cutaneous nerve under the inguinal ligament.
A 72-year-old man presented with increasing left groin and upper thigh pain that had begun 1 week previously. Deep venous phlebitis was diagnosed, and the patient was treated with anticoagulation. Partial thromboplastin time and prothrombin time were well maintained. Four days later, the patient experienced left flank pain radiating into his left thigh that in a few days became more severe and extended below his knee into the medial leg. He could not raise his left leg off the bed. There was no back pain, radicular pain or sphincter dysfunction.
Neurologic examination demonstrated moderately severe weakness of the left iliopsoas and quadriceps muscles, absent left quadriceps muscle stretch reflex, and diminished sensation to touch and pinprick over the anterior thigh and medial leg below the knee.
--What is the diagnosis in this case?
Obturator nerve compression
Femoral nerve compression
Lumbosacral plexus compression
Sciatic nerve compression
L2 - L3 nerve root compression
--Femoral Nerve compression--
B: Pelvic CT demonstrated asymmetric enlargement of the left iliacus and psoas muscles in the pelvis, consistent with a hemorrhage. Surgery revealed a large hematomas that medially compressed the femoral nerve. This was successfully drained. Postoperatively, the patient gradually improved, regaining significant function within a week.
A 51 year old male presented with a five year history of intermittent numbness in his left foot on the medial aspect. Recently pain has developed and he stated it's a "sharp knifelike pain" associated with numbness on the sole of his foot. The pain wakes him at night on occasion. He describes the pain increased the more he was on it, mostly in the afternoon and that it was not as bad at the beginning of the day. The neurological exam was normal except pain was elicited with inversion of the foot.
--Based on the above history, you suspect?
Tarsal tunnel syndrome
Lateral ligamentous sprain
Neuroma of the plantar digital nerves
B, Tarsal tunnel syndrome. The patient may or may not have a positive Tinel's sign over the nerve as it passes under the flexor reticulum at the medial malleolus. Sensory nerve conduction of the medial and lateral plantar nerves are slow across the reticulum. The fact that the pain is worse as the day progresses should alert you to its presence. Plantar fasciitis, on the other hand, causes pain immediately when the patient stands to dress in the morning.
A 62 year old insulin dependent diabetic female. Was sitting at home and she fell when getting up to go to the bathroom. She states that her right knee buckled. She also described a mild right groin pain which radiated into the thigh. She also noticed some numbness in the medial lower leg. She has no other complaints. Your examination was normal except for a mild weakness 4/5 of her right quadriceps and a decreased patellar reflex.
--You suspect which of the following occurred.
Ischemic damage to the femoral nerve
Hemorrhage into the obturator nerve
L 4 nerve root compression
Cauda equina syndrome
Femoral nerve ischemia due to vasa nervorum damage from diabetes. Although not frequently seen is a major cause of femoral mononeuropathy. If a hemorrhage into the nerve had occurred there would be severe pain not mild. The obturator nerve supplies the adductor thigh muscles which were normal in this patient. Femoral ischemic neuropathy may recover completely in 3 - 6 months depending on the degree of damage and will the patient will require rehabilitation.
THIS SET IS OFTEN IN FOLDERS WITH...
First Aid for USMLE-micro
First Aid Psychiatry
ARF/AKI: Pathoma & Prabhaker & Tran
YOU MIGHT ALSO LIKE...
Final - 4/9/18 - Disorders of the PNS
Exam 3: Alterations in Neurologic Functi…
5/30 - Intro to Screening for Medical Disease in a…
OTHER SETS BY THIS CREATOR
Q4 Neuro Brainstem
Q4 Path / Neuro
Micro Q3-B3 Parasites