Introduction To Clinical Medicine (ICM) : Case Studies Neurologic Disorders
Introduction To Clinical Medicine (ICM) : Case Studies Neurologic Disorders
Introduction To Clinical Medicine (ICM) : Case Studies Neurologic Disorders
(ICM)
Case studies
Neurologic Disorders
Prepared by:
Robert W. Wilhoite M.D.
Edited by
Patrice Thibodeau, M.D.
Notes for next semester
• Lots or repetition about ICP
• Look into why LP is therapeutic for a patient with patient with Pseudotumor cerebri who
has increased pressure, but LP can cause herniation if done with increased ICP. (is is
because there is a shift and blood in patient with ICH and not with patient with
Pseudotumor cerebri?
• There seems to be a lot of repetition from morning to afternoon, but the students were
ok with this when asked.
• May want to try to make the cases less obvious and ask students for next steps..etc.
• Get rid of the case numbers on each slide
• Look up meningtitis vs encephalitis and change in mental status? Seen in meningitis?
Case # 1
• This 62 year old right-handed white male
suddenly developed difficulty speaking fluently
and experienced a weakness in his right facial
muscles and right arm with normal function of
lower extremities.
• Vital signs: temp 98.6, BP of 150/86, HR 86 RR 14
• Neurologic exam: revealed 3/5 motor in all
muscles of the right upper extremity, and the
following visual field cuts:
– Hemorrhagic stroke
• SAH – AV malformation
• ICH
– Tumor
How would you proceed in your evaluation
of a patient with a potential stroke ?
• Neurologic examination
• CT scan of the head to rule out hemorrhage (ICH)
and look at size of defect if present on CT.
• If suspect SAH, but do not see bleed, then need to
do LP to rule out.
• Establish if patient is candidate for IV
thrombolysis (see morning lecture)
• ECG – cardiac arrhythmia / recent MI
• CBC (platelets), PTT, PT (needed for exclusion
criteria)
Case # 1
• How would you acutely treat this patient?
– Depends on etiology: Must r.o. hemorrhage
first!
– If hemorrhagic – emergent neurosurgery
consult
– If ischemic stroke
• Intravenous thrombolytic therapy if no
contraindications for thrombolysis
– Tissue plasminogen activator (tPA)
– Must start within 3 hours
Stroke
3rd leading cause of death
• Types of stroke and characteristics:
– Cerebral infarct:
• Etiology: thrombosis or embolization
• Abrupt onset
• S & S – vary with vessel involvement as noted in
previous slides
Types of stroke
– Cerebral hemorrhage:
• Etiology :
– HTN
– Aneurysm
– Bleeding disorder
• S&S
– Nausea, vomiting, headache
– Neurologic deficit with hemiplegia
– Nuchal rigidity
– Impaired consciousness leading to coma
Final diagnosis
Intracerebral infarct
due to
occlusion of left middle cerebral
artery
Case # 2
• This 18 year old college student was
mugged on her way home from class. She
was severely beaten on the head and
shoulders.
• In the ER the patient appeared confused
and complained of severe headache. On
PE of the head you feel a depression in
the right frontal skull and suspect a skull
fracture. There are no raccoon eyes or
Battle sign.
Case # 2
• Findings:
– Confusion
– Headache
– ? Skull fracture
– No raccoon eyes or Battle sign
Case # 2
• What is your differential diagnosis?
– Subdural hematoma
– Epidural hematoma
What are the various types of
intracranial hemorrhage?
– Epidural
– Subdural
– Subarachnoid
– Intracerebral
– Intraventricular
What are the various meningial
layers covering the brain?
– Pia mater
• Innermost layer
directly attached to
the brain
– Arachnoid
• Middle layer which
envelopes the CSF
• Subarachnoid space –
circulating CSF
– Dura mater
• Fibrous outermost
layer – anchors
meninges to skull
Acute epidural hemorrhage
– Usually result of direct injury
to the head (trauma) Epidural
– Skull fracture usually present
– Tear in the middle meningeal
artery leading to football
shaped hematoma against
smooth dura which is visible
on CT scan
– Bleed is brisk from artery
– Short lucid period and quick
lapse into coma due to brain
compression from expanding
hematoma
– Headache/Confusion
– Seizures hours after injury
Epidural hematoma
Dura mater
Acute subdural hemorrhage
– Most common cause: trauma
– Results from a tear in bridging
veins and subsequent expansion
of blood clot which is crescent
shaped and follows the convexity
of the brain tissue.
– Direct head trauma or
acceleration forces as in whiplash
– Symptom onset varies from
hours to weeks because the
bleeding is venous. Slower.
– 1/3 of patients will have a lucid
period before slipping into coma
– Gradual increasing HA and
confusionLOCcomatose
Reflected dura mater
Bridging veins
Subdural hemorrhage
Dura mater
Chronic subdural hemorrhage
• Commonly seen in the elderly
• Injury may be trivial and forgotten
• Elderly have general loss of brain volume/atrophy thus
longer for symptoms to occur
• Central bridging veins more exposed to trauma in elderly
• Manifests as altered mental status, slowed thinking, vague
change in personality, seizure and sometimes focal neurologic
findings.
• May be misdiagnosed as dementia, stroke, brain tumor,
depression because the drowsiness, incoherence and
inattentiveness are more prominent than focal signs such as
hemiparesis.
Case # 2
What additional studies would you order
for our patient?
– CT scan
How could you identify a
basilar skull fracture?
Epidural hemorrhage
Case # 3
• This 32 year old woman complained of a sudden
onset of severe headache, dizziness and vertigo
following which she became unconscious.
• Physical exam revealed some rigidity of her neck,
ophthalmic exam showed equal pupils and no
evidence of papilledema.
• Within the next two hours she suffered a mild
seizure following which she became apneic and
was unable to be resuscitated.
Case # 3
• Findings:
– Headache, dizziness and vertigo
– Neck rigidity
– No papilledema
– Seizure and apnea
– FH of PCKD
Case # 3
• What is your differential diagnosis?
– Subarachnoid hemorrhage
– Intracranial lesion
– Meningitis
What if you were told:
• FH is significant for PCKD in mother
and sister
Acute subarachnoid hemorrhage
• Most common cause is
ruptured intracranial
aneurysms
• Bleeding occurs in the
subarachnoid space
where the CSF is found.
(LP is important)
• Presents as “Worse
headache I’ve ever had!”
Subarachnoid hemorrhage from Berry aneurysm
Note: No blood beneath the dura
Subarachnoid hemorrage
Case # 3
• How would you have initially evaluated this
patient?
– Complete neurologic exam
– Immediate CT of brain
– If no evidence of hemorrhage or increased
intracranial pressure on CT, perform lumbar
puncture looking for blood or xanthrochromia
– Contraindications for Lumbar puncture?
– MRI is less sensitive than CT
– Cerebral angiography or CTA – may be used in
patient with neg CT and equivocal LP results
Cushing Triad
• A sign of increased ICP and imminent brain
herniation
– HTN
– Bradycardia
– Hyponea/apnea
Intracerebral hemorrhage
due to
Coumadin overdose
Case # 5
• This 42 year old man suffered a seizure
and became semi-conscious.
• Physical exam revealed 3+ papilledema.
• A chest x-ray showed a mass in the left
upper lobe of his lung and biopsy was
read as small cell carcinoma.
• His condition did not improve and he
quietly expired 12 hours later.
Case # 5
– Laboratory findings revealed the following:
• Serum osmolality 200 mosmo/kg (low)
• Serum sodium 128 mEq/liter
• Urine osmolality-elevated
• ADH – elevated
• Spinal tap showed a pressure of 200
• CSF fluid showed a few mononuclear cells
• The gross picture is of his brain.
Case # 5
• Findings:
– Seizure
– Papilledema
– Mass in the lung
– Hypo-osmolar hyponatremia with elevated
ADH.
Case # 5
1. What is your differential diagnosis?
– SIADH causing cerebral edema
2. What is your interpretation of the laboratory
findings?
– Serum osmolality –low –ADH retains water
– Urine osmolality – high –lack of water excretion
– Serum sodium – low (dilutional hyponatremia)
– Consistent with SIADH
3. Why does this patient have SIADH?
Case # 5
• What are the signs of increased intracranial
pressure?
– Headache
– Nausea
– Vomiting
– Papilledema
– Decreased arousal
– Cranial nerve palsies
– Coma
Complications of increased
intracranial pressure
• Kernig’s sign:
– Extension of knee with hip at 90 degree
flexion causes pain in hamstring muscles and
resistance.
• Brudzinski’s sign:
– Flexion of neck causes flexion of the hips and
knees
Case # 6
• How would you proceed in your evaluation of this
patient?
• CT – r.o. increased intracranial pressure (has
mental status changes so must do CT before LP)
• Lumbar puncture
– Opening pressure
– Cell count
– Protein, glucose
– CSF Culture and gram stain
– HSV PCR
• Blood culture
Case # 6
• What is your differential diagnosis?
– Bacterial meningitis
– Viral meningitis
– Meningoencephalitis
• How would you attempt to differentiate the
bacterial vs viral meningitis?
– Check CSF differential smear –PMN’s vesus Lymphs
– Gram stain
– Blood culture
– Decreased glucose and increased protein
Case # 6
Appearance Prot. Glucose WBC RBC
Nml clear 15-40 50-70 <5 0
Bacterial meningitis
Case # 7
• This 69 year old man is brought to his PCP by
his wife. She states that he manifests increasing
mood swings and forgetfullness. Several
months ago he experienced angry outbursts
with his employees although the patient denies
such charges. His memory of acute events is
diminished.
• General physical and neurologic exams are
non-contributory.
Case # 7
• Findings:
– Mood swings
– Memory loss
Case # 7
• What is the basic consideration in the
evaluation of this patient?
– He manifests a chronic progressive dementia
– What is your differential diagnosis?
• Alzeimer’s disease (long periods of symptoms)
• Lewy Body disease i.e. Parkinson’s disease (rigidity,
tremors)
• Multi-infarct dementia
• Normal pressure hydrocephalus
• Dementia due to infections (HIV, viral)
• Metabolic disease (hypothyroid, B12 def.)
• Toxins (alcohol, arsenic, mercury)
• Depression
Case # 7
• What procedures would you utilize in your
evaluation of this case?
– CBC, TSH, B 12
– BMP would be reasonable as a baseline
– Urine toxicology screen
– HIV and VDRL if has risks
– CT scan - rule out tumor and normal pressure
hydrocephalus
Case # 7
What is your working diagnosis?
Dementia
Alzheimer’s disease
Signs and Symptoms
of Alzheimer’s disease
• Loss of memory – seen in 10 % over 70
years of age and is part of normal aging
• May be episodic
• Change of environment –e.g. become lost
• Personality changes –aggressive behavior
Cerebral atrophy
Cerebral cortical atrophy with ventricular dilatation
Alzheimer's disease
Final diagnosis
Alzheimer’s disease
Case # 8
• This 66 year old woman presents with fever,
seizures and altered consciousness.
• She has been ill over the past two days with
fever, headaches and fatigue. The morning of
admission her husband tried to wake her but
she appeared confused, incoherent and then
had two generalized seizures each lasting 2-3
minutes. She has not regained normal
mentation since then.
• Past history: no prior history of seizures or
headaches.
• On PE: the patient is agitated and
muttering incoherently.
• CN II-XII are intact.
• She is moving all 4 extremities and
withdraws all four limbs to pain.
Labs
HSV encephalitis
Case # 9
• This 36 year old woman, a computer technologist,
consults with her PCP because of a sudden episode of
“double vision.” She is concerned that she may be
having a stroke. She has been under increasing
pressure at her job and recently has felt tired and
clumsy.
• One year ago she experienced a single episode of
numbness in her right foot but this lasted for only two
days.
• Physical exam reveals some nystagmus and increased
deep tendon reflexes in her left leg with some weakness
in that leg. Sensations in that leg are described as
normal.
Case # 9
• What is your differential diagnosis?
– Multiple sclerosis
– Myasthenia gravis
– Guillain-Barre syndrome
– Polyneuropathy
Case # 9
• How would you proceed in your evaluation of
this case?
– Complete neurologic exam
– MRI
• may show periventricular, juxtacortical, infratentorial
(brainstem and cerebellum), spinal cord plaques
– Lumbar puncture- ? tests
• Opening pressure
• Pleocytosis with elevated lymphocytes
• Increased protein with increased IgG index
• Electrophoresis for oligoclonal banding
Case # 9
• How would you define multiple sclerosis?
– A progressive demyelination throughout the
central nervous system thought to be due to
an autoimmune process.
– It is characterized by a loss of
oligodendroglial cells around the myelin
sheaths and replacement with fibrous glial
scar resulting in impaired axonal
conduction.
Case # 9
• Characteristics of multiple sclerosis:
– Usually affects young women 20-50 years old
– Transitory and scattered neurologic defects
– Exacerbated with infections, stress or
elevated body temperature (Uhthoff
phenomenon)
– Most common presentations: paresthesias,
weakness, abnormal gait and visual loss
– Symptoms wax and wane
Final diagnosis
Multiple sclerosis
Case # 10
• This 26 year old woman has noted blurry vision
and progressive weakness in chewing her food.
She runs 2 miles a day in the morning and
states that her leg muscles seem to lose their
strength after the first mile.
• Physical exam reveals some nystagmus and
slight ptosis. Deep tendon reflexes are normal
• BP 120/82
Case # 10
• Findings:
– Progressive weakness in chewing her food
– Increased muscle weakness with challenge
– Diplopia
– Nystagmus
– Slight ptosis
Case # 10
• What is your differential diagnosis?
– Myasthenia gravis
– Thymoma
– Lambert-Eaton syndrome
– Temporal arteritis
Case # 10
• What tests would you order in the
evaluation of this case?
– CT of chest to r.o. thymoma
– Check acetylcholine receptor antibodies
– EMG
Case # 10
• What is the basic defect in myasthenia gravis?
– Autoimmune disease directed at the postsynaptic
neuromuscular junction (the acetylcholine receptors)
• What are the common symptoms seen in this
disease?
– Fluctuating, painless and fatigable weakness involving
the ocular, bulbar, cervical, limb and respiratory
muscle.
Case # 10
• The origin of the antibodies is unclear.
• First line treatment options
– Cholinesterase inhibitor pyridostigmine
– Glucocorticoids
– Immunosuppressant agents (azathioprine,
cyclosporine, mycophenolate mofetil)
– May use IV IG or plasmapheresis in acute
treatment before using glucocorticoids
• Thymectomy may result in a lessening of
symptoms.
Final diagnosis
Myasthenia gravis
Case # 11
• This 23 year old woman has an 8 month history
of headaches. Initially they occurred
sporadically but in the past 2 months they have
become more frequent now occurring once a
week. Associated with these attacks she is
nauseous and occasionally vomits. Her
headaches consists of throbbing pain over her
temple area. Although OTC meds help she
prefers to “sleep it off” in a dark, quiet room.
• A neurologic exam is within normal limits.
Case #11
• How would you evaluate a patient with
headaches?
– Ask:
• Frequency
• Duration
• Evolution in time
• Location of any pain
• Trigger mechanisms
• Neurologic exam
Case # 11
• Precipitating factors may offer a clue to the
diagnosis!
– Recent sinusitis, hay fever, dental surgery, head
injury or sysptoms of viral infection
– Migraine exacerbated by emotional stress or foods
– Alcohol may cause cluster headaches
– Temporomandibular joint dysfunction –facial pain
or upon chewing
– Masticatory claudication – temporal arteritis
Case # 11
• What is your differential diagnosis in this case?
– Migraine headache
– Cluster headache
• Unilateral, retro-orbital, abrupt, (within min.)
– Tension headache
• Bilateral , arise in temporal area /back of head, gradual
– Subarachnoid hemorrhage
• “Worst headache of my life!”
– Intracranial lesion (tumor, abscess)
• Progressive
– Meningitis
Case # 11
• Migraine headaches:
– Classic findings:
• Cannot tolerate loud sounds or bright lights
• Prior to onset experience bright lights in front of
her eyes as if zigzagging across her field of vision
• Trigger mechanisms:
– Red wine, ripened cheese, Chinese food
(MSG), chocolate
How would you treat this patient?
• Abortive? Preventative? Or both?
Final diagnosis
Migraine headaches