Neurology Review

NEUROLOGY
MOTOR OR PYRAMIDAL SYSTEM
 Consists of neurons whose cell bodies are in the motor cortex (precentral sulcus).
 This system of neurons runs its fibers through the white matter of the brain, around the
ventricles, and the fibers cross in the medulla.
 On the motor cortex, these fibers are separated into what’s called the Motor Homunculus
Motor Homunculus
 The face, the arm representation is found laterally

o The middle cerebral artery supplies to the lateral region
 The leg & genital fibers are in the parasagital region &Torso is at the central part of the brain
o Anterior cerebral artery supplies the middle region where the leg fibers are
 Stroke due to:

o Middle cerebral artery infarction  Face and arm weakness > the leg
o Anterior cerebral artery infarction  leg is weak but their face and arm are spared
 Normal pressure Hydrocephalus  affect the face area of internal capsule which is close to
the ventricles
o Internal capsule received blood from branches of Middle cerebral artery
 In the internal capsule region, the face arm and leg fibers are very close together, and if
someone has weakness equally in all of these areas, you can pinpoint that to the internal
capsule (lacunar infarction), or to the brainstem. Face, arm & leg are equally involved
 Pons lesions will affect the cerebellum  Ataxia in addition to weakness of face, arm & leg
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 The left hemisphere is involved mostly with language
 The right hemisphere is involved with spatial relationships.
 Cortical phenomenon:
o Weakness in the face & arm > leg
o Aphasia
 Upper motor neuron: Starts from the cerebral motor cortex  cross at the end of the medulla
 Anterior horn cells. They synapse with the cells of the anterior horn.
o Upper neuron lesion will produce weakness of the limb & hyperreflexia (deep tendon
reflexes) + Babinski sign.
 Lower motor neuron goes from anterior horn cells out to the neuromuscular junction.
 A lower neuron lesion will produce weakness of the limb & lack of reflexes. (eg could be
due to herniated disc in the back, or entrapment).
 Weakness also maybe due to Neuro-Muscular junction problems or due atrophy of muscles
itself.
Sensory Pathways
 Posterior column - involved with vibration & proprioception - cross in the medulla (MLF)
 Lateral Spinothalamic tract - pain & temperature (pinprick) – cross on the same level of
spinal cord (within 2-3 levels)
 These two systems project to the thalamus  Internal Capsule  postcentral gyrus
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Brown-Sequard - Hemisection of the spinal cord ------------------------------------------------------ *** TQ
  weakness on same side

  vibration and proprioception loss on same side
  pain and temp loss on opposite side
Cranial Nerves
 III, IV, VI - occulomotor movements

 III CN
o Pupillary nerve fibers (Parasympathetic) run on the outside of the nerve and the
occulomotor fibers run on the inside of the III nerve -------------------------------- *** TQ
o Compression affects outside of nerve more (in increased ICP)  cause dilation of
pupils(parasympathetic innervation carried by this nerve usually makes pupils smaller) but
doesn’t affect the eye movements)
 e.g. - herniation of temporal lobe compresses nerve III
 This is a Neurological emergency - need to find a way to decrease the pressure,
because if pressure continues to build up, it cuts off the blood supply to the brain
and the brain tissue will die.
o Diabetes affects middle of nerve more (by ischemia)  cause paralysis of eye movements
(eyes look down and out) but spare the pupils ------------------------------------------ *** TQ
o In DM, microinfarcts are common - it’s not unusual to have nerve infarcts (eg III CN infarct)
o Typically these things get better on their own within a few weeks.
 Because of proximity of third nerve nucleous & red nucleus
o In brain stem infarct  affect rubrothalamic tract (cerebellum ⇒ pons ⇒ thalamus) 
Tremors & Ataxia with III nerve pulsy (Benedict Syndrome)
o If you lesion in the midbrain that affect the III nerve nucleous & Cortico-Spinal tract,
but spare the red nucleous  Weber’s Syndrome  hemiparesis & III palsy
 Pican Aneurysm: Post communicating Artery Aneurysm  cause compression of III nerve
 V CN - Sensation to the face

o V - nucleus (principle sensory) very long. Some rare cases can have sensory loss on right
side of face from right sided lesion. (usually opp side though)
o Cervical spinal cord lesion may cause face numbness due to trigeminal spinal tract that
involved in pinprick sensation to the face.
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 VI CN
o Gradenigo syndrome - Inflammation of the petrous part of the temporal bone  some
abducens paralysis.
 VII CN - facial motion

o Stroke  (UMN)  lower facial paralysis, but eye movements spared (III CN is intact)
o Bells Palsy (LMN)
  upper & lower facial paralysis (Herpes Virus at geniculate ganglion level)
  Absent sense of taste from ant 2/3 (chorda tympani)
  Hyperaccousis (because VII innervate the trapisus muscle near
the tympanic membrane  tension to tympanic membrane, if so, lesion is
probably around internal auditory meatus, and not in the brainstem)
Cavernous sinus - III, IV, V1, VI and sympathetic innervation to carotid ---------------------------- *** TQ
o Tumors (Cranio-Pharyngeoma) of the cavernous sinus  affect these nerves.
o Talusa Hunt Syndrome (Inflammation of the cavernous sinus)  also affect these nerves
Cerebellum - (important in coordination) right hemisphere controls right side, and vice versa, due to
double crossover of fibers.
Visual System
 Right visual field projects to the left part of the retina
 In general, the left occipital lobe and the left retina are involved with seeing things on the right
side of the face and vice versa.
 A stroke affecting the left occipital lobe will cause loss of vision in the right side of the face.
 Pituitary tumor around the optic chiasm will cause a bitemporal hemianopsia
 Retinal problems - will have islets of visual problems - not broken up as neatly as neural
problems.
 Macular vision is the central area of vision -------------------------------------------------- *** TQ
o It is the most important part of vision and it projects to the macular region at the tip of the
occipital lobe
 Generalized Hypoperfusion Syndrome
o Due to dropping of the BP
o  area that’s furthest away from the circulation, ie (area between Vertebral a. & PCA
will be affected first “Watershed infarction”  (eg - Lt. or Rt. occipital area) 
Macular visual loss & Transcortical Aphasia)
o OR  area between ACA & MCA will be affected first “Watershed infarction” 
Proximal arm/shoulder motor loss: Think of motor homunculus - Face and arm are
affected by middle cerebral artery, leg involved with anterior cerebral artery & the
watershed area in the cortex supplies the shoulder area (causes “man in the barrel”
syndrome)
 Occlusion of L posterior cerebral a. - occipital tip is spared - i.e. macular vission sparing
 Visual Exam (Funds)
o Macula - paling of disc seen with demyelinating disorders
o Macular vision loss (Macular Scottoma) can occur in migraine
o Swelling seen with tumors (papilledema)
o Visual loss can be with swelling of the disc or not.
o If there is disc edema & patient > 60 y.o.  Ischemia of the optic nerve (Painless)
o If there is disc edema & patient in 20’s y.o.  Demylination of the optic nerve (MS)
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o If there is No disc edema  Central retinal Artery occlusion (CRAO): 25 % due to Carotid
emboli, 25 % due to Lupus (or other arteritis such as temporal)
 Temporal Artritis (Painfull)  infarction of optic nerve  loss of vision
o If bilateral disc edema without visual loss  Papil edema (Painless)
 Sympathetic innervation of eye - causes dilation - three neurons are involved:
 I neuron - posterior hypothalamus  upper spinal cord (C8-T2 level)
 2 neuron - upper spinal cord (C8-T2 level) - across apex of lung to internal carotid a.
 3 neuron - Superior cervical ganglion
  pupillary motor fibers
o Horner’s syndrome - pupil is abnormally constricted with ptosis
 Use Cocaine then hydroxyamphetamine/cocaine to test pupil: cause release of
Epinephrine (normally would make it dilate)
 Introduce drug into pupil to determine which of the three neurons has been
affected.
 If lesion is 1st or 2nd order - dilation will occur with medications
 If lesion is 3rd order - no dilation will occur with medications
 This test is to defirenciate whether the lesion from brain stem or Apex lung TB or
neck lesion 1,2 D - 3 ND ----------------------------------------------------------- *** TQ
 Pupils should be equally reactive to light and accommodation
 Accommodation: Light in one eye cause constriction of the other eye’s pupil
 Afferent pupillary defect  visual acuity defect because it involves the optic nerve directly
o Normally the pupils dilate right away and then rebound a little bit.
o If there is a problem with communication between retina and PSNS and SNS, then this is
called an afferent pupillary defect.
o Marcus Gunn pupil  Afferent pupillary defect (don’t get constriction of pupils if you
shine the light) - caused by Demyelination of optic nerve
 Medial Longitudinal fasciculus
o Connects head & neck motion to eye movements (ie connects vestibular nucleus
(parapontine reticular formation - PPRF to III & VI nuclei)
o Necessary to track objects with eyes movements (Congrugate together - Movements of
one eye is in senchrony with the other eye)
o If there is dis-Congrugate movements then it is a lesion at the brain stem level ***TQ
o To test this clinically by Ice water caloric test:
 Test the unresponsive patient: Squirt ice water into ear  eyes will gradually move
over to that side, followed by a rapid corrective nystagmus to opposite side.
 This tests the vestibular connections between the III and VI nerve.
• Identifies lesions of MLF (if only one eye moves & the other eye stays in
midline you know there is a lesion). (very potent stimulus - can agitate
brain dead patients) mnemonic: cold opposite warm same (“COWS”)
o Also can be tested by Doll’s eyes maneuver (move the head to one side then the other
Normal EEG patterns

o α : 8 - 13 Hz (awake with closing eyes)
o β : 14 - 35 Hz (awake with open eyes)
o Theta: 4 - 7 Hz
o Delta(δ) < 4 Hz
o POSTS Spindles, K-Complex & Vertex Sharp (during REM sleep)
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STROKE
Definition
 Stroke = Acute disruption of blood flow to the brain leading to focal neurologic deficits
 TIA (transient ischemic attack) = Acute disruption of blood flow to the brain leading to focal
neurologic deficits lasting less than 24 hours (usually 3 – 10 minutes)
 Usually the emboli from the heart or internal carotid artery (must do surgery if stenosis of
internal carotid artery > 70%)
 TIA of left internal carotid artery  left eye vision loss (due to occlusion of left Ophthalmic
Artery) + right face weakness + slert of speech, then weakness of right side of the body (due to
occlusion of left Middle cerebral artey)
 Rx: Heparin then surgery if occlusion > 70%
 Rx of TIA of Vertebrobasilar system: No surgery, Cumudine
 Crushendo TIA: multiple TIA’s that will lead to Stroke if not treated (Emergency admission to
hospital)
 Dissection of Internal Carotid Artery (due to trauma)  clot goes to inside the artery 
Horner Syndrome ------------------------------------------------------------------------------- ***TQ
o Rx: Heparin or Cumodine to prevent clotting
Epidemiology
 700,000 stroke per year (Ischemic Strokes - 80%: 1/2 - small vessels & 1/2 - large vessels)
 Leading cause of disability in USA
 Incidence increases with age
 African Americans > Hispanics > Whites
Stroke subtypes
 Ischemic (large & small vessels clots)
 Hemorrhagic (Aneurysm rupture or Arterio-Venous malformation ruptures)
 Superior Sagital Sinus thrombosis (Rare)
o Usually happens in people who have hyper-coagulative states (post partum and Multiple myloma)
o  Blood will not be able to drain into the sagital sinus  infarction of the top of the brain 
bilateral hemispheric infarctions
o Rx: Anti coagulants
Ischemic Stroke Subtypes

 Thrombotic: a blood clot forms within a blood vessel in the brain
 Embolic: a blood clot forms within the heart or a major blood vessel of the brain
 Lacunar: a very small blood vessel of the brain progressively narrows until completely occluded due
to Lipo-Hylenosis of small vessels ---------------------------------------------------------------------- ***TQ
 Cryptogenic: the mechanism for the stroke is unknown
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Stroke Syndromes
Lacunar syndromes: (small vessels clots) ---------------------------------------------------------------- *** TQ

 Due to Lipo-Hylenosis
 No cortical involvement
 Syndromes according to location:
o Pure motor Hemi-plegia (Most common): face, arm & leg are equally involved without
cortical syndromes (NO Aphasia)
  Face, arm & leg are equally involved if stroke in the internal capsule or cortico
spinal tract (specially in Pons)
o Pure sensory loss: lesion in Thalamus
o Ataxia hemiparesis: lesion in the Pons
o Dysarthria clumsy-hand: lesion in the Pons
o Sensorimotor
 Rx: Aspirin
Large vessel strokes (Cortical Strokes)

 Invoved the internal carotid artery and its branches
 Usually due to emboli from the heart (Atrial fibrillation or Mitral valve stenosis)  the clot
travel to the carotid artery
 Mostly involved the Middle cerebral artery
 Anterior cerebral artery: (in between the two hemishers)
o Occlusion of left ACA 
 Weakness of right lower limb (right side of face usually spared & right upper
limb less affected than right lower limb)
 Speech disturbance (dysphasia)
 Apraxia of left (non paralyzed) side of body (apraxia = inability to properly
execute movements despite normal strength)
 Disturbance of bladder control
 Confusion initially, later personality change may occur
 Middle cerebral artery – non-dominant (right hemisphere stroke in right handed person)
o Weakness of left side of face & left arm (left leg less affected)
o Left sided sensory disturbance
o Visual disturbance: loss of lower left part of field of vision of each eye (homonymous left
lower quadrantanopia)
o Confusion, sensory and/or motor neglect
 Middle cerebral artery – dominant (left hemisphere stroke in most people)
o Weakness of right side of face & right arm (right leg less affected)
o Sensory impairment right side of body
o Speech disturbance (dysphasia), & difficulty in comprehending written words & writing
o Visual field loss in lower right quadrant of visual field of each eye (homonymous right
lower quadrantanopia)
 MCA Stem disease ------------------------------------------------------------------------------ *** TQ
o Occlusion of MCA stem: just before division of MCA to Superior & Inferior Braches
o No Surgical treatment
• > 70% Cumudine
• < 70 % - Aspirin
o Remember ----------------------------------------------------------------------------------- *** TQ
 MCA - Superior Branch supply  Broca’s area
 MCA - Inferior Branch supply  Wernicke area
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 Vertebrobasilar system
o Basilar artery:
 Complete obstruction of the basilar artery is usually rapidly fatal, with rapid onset
of unconsciousness and deepening coma.
 Small branch occlusions
• In the pons:
• Sixth nerve under action on the side of stroke, weakness of arm and leg on
side opposite stroke, impaired conjugate gaze
o In the midbrain:
 Third nerve impairment on side of stroke, weakness of arm and leg on side opposite
to stroke
o Posterior cerebral artery:
 Loss of half of the field of vision on the side opposite to the stroke (homonymous
hemianopia)
 Ischemic injury to the thalamus may result in unpleasant, burning pain over
opposite side of body (thalamic syndrome)
o Vertebral artery:
 Vertigo at onset
 Cerebellar incoordination of arm and leg on the same side
 Loss of pain and temperature sense of the half of the face that is on the same side as
the stroke, and of the trunk and limbs on the side opposite to the stroke
 Difficulty in swallowing and speaking
 Horner’s syndrome (small pupil, mild drooping of eyelid and lack of sweating of
face on same side as stroke)
Evaluation of acute stroke patients

 Medical evaluation
 Neurologic evaluation
o Mental status
o Cranial nerves
o Motor
o Sensory
o Coordination
o Gait
 Laboratories
 Imaging
o Non-contrast head CT
o MRI
 Diffusion/perfusion weighting
 MRA
o Carotid ultrasound
o Echocardiogram/EKG
o Angiography
Treatment of acute stroke patients

 Urgent general supportive care
 Management of serum glucose
 Management of hypertension
 Seizure management
 Management of brain edema
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 Medications (only within 3 hours of developing the Ischemic Stroke):
o Intravenous t-PA
o Intra-arterial t-PA
o Anticoagulation
o t-PA complications  Bleeding in 25% treated cases
o Inclusion Criteria for t-PA treatment -------------------------------------------------- *** TQ
 18 y.o.
 Ischemic Stroke
 Measurable neurological defects
 Stroke occur < 3 hours
 CT scan shows no bleeding
o Exclusion Criteria for t-PA treatment
 History of Surgery or Trauma within few weeks
 History of bleedings
 History of HBP
 History of Seizures
 History of infections
 History of other Strokes
 CT scan shows bleedings
 Glucose < 50, or > 400
 Platelets < 100
 Acute MI
 Pregnancy or lactation females
 Any oral Anticoagulation
Hemorrhagic Stroke
 Due to Aneurysm rupture or Arterio-Venous malformation ruptures
o Aneurysm location mostly occur in the anterior circulation: anterior communicating artery 30%,
anterior, middle cerebral artery 30% & posterior cerebral artery 30% (least in basilar artery <
15%)
 Most patients with Aneurysm ruptures dies or if survive will have permanent neurological
defects
 Rx if survive:
• Platelets
• Keep the person perfused (Hydration)
• Prevent spasms of surrounding blood vessels (motopine)
 The most important to remember (Worst headache in my life: Emergency) --------*** TQ
• CT scan
• Lumber puncture
• MRA
o Arterio-Venous malformation
 May present with bleedings or seizures
 May be gradual developments of neurological deficits
Complications of acute hemorrhagic stroke

 Thrombotic complications
 Medical complications
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Risk factors of hemorrhagic stroke
 Hypertension
 Cigarette smoking
 Alcohol use
 ⇓ Physical activity
 High cholesterol (Hyperlipidemia)
 Atrial fibrillation
 Transient ischemic attacks
Treatment/medications for hemorrhagic stroke

 Antiplatelet therapy
 Anticoagulation
 Other
Storkes in children and young adults

 Atherosclerosis
 Embolism (from heart or Rt to Lt paradoxical embolism from patent foramen ovale)
 Arteropathy
o Inflammatory
 Takayashu Aortitis: inflammation of Aorta (Remember: Talusa Hunt -
inflammation of Cavernous sinusis)
 Syphilis
 AIDS
 Collagen
 Vascular Diseases
 Allergies
 Amphetamines
o Non-Inflammatory
 Dissection of Carotid Artery
 Moya-Moya Disease (abnormal collection of blood vessels in the base of the
brain): look like MS with alterations of attacks and remissions.
 Fibromuscular Dysplasia
 Radiation Therapy
 Vasospasm
 Hematologic (in Hyper-coagulation states)
 Metabolic disorders (Homocystine abnormalities or Fabre disease)
 Venous (sagital sinus thrombosis)
 Trauma (sub- & epi-dural hematomas)
 Hypeoperfusion: Watershed infarct (from decreased blood pressure)
Carotid artery dissection - with trauma get blood in lumen and wall of artery can prduce the emboli. Put
them on thinners
Bruit in Carotid Artery indicates stenosis. If its asymptomatic don’t do anything for it. (some
physicians will perform surgery even if asymptomatic when stenosis > 70%: I prefer surgery)
Subclavian Steal syndrome - Narrowing of artery proximal to origin of vertebnral artery. May have TIA
of the vertebral artery when exercising (The arm steal blood from vertebral artery).
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EPILEPSY
Seizures
 Electrical discharge in CNS (due to irritation of cortex).
 Different areas of brain produce different symptoms
Two major groups

 Focal (Partial): generated by one area of brain, it can lead to generalized (via Corpus
Collusum)
o Simple - no loss of consciousness
o Complex - loss of consciousness is present
 Generalized
o Absence (Petit mal)
o Grand mal (Tonic-Clonic)
o Myoclonic
o Atonic: When prefrontal cortex is stimulated  weird symptoms
Types of Seizures
Infantile Spasm (West Disease)

 Shock like flexor spasm
 Onset: 3-8 month old onset
 Causes: 40% idiopathic & 60% due to metabolic, cerebral malformation, infection or trauma
 Prognosis is poor 90% retarded, 20% die due to derangement.
 EEG pattern:
o Hippsarythmia - poorly organized, waves are slow, high voltage, spikes & slow waves
(separated spikes). ---------------------------------------------------------------------------- ***TQ
 Rx:
o Prednisone & ACTH (The only disorder treated with steroids)
o Pyrodoxin Challange (Try to stop the seizures during EEG)
o Valproic Acid & Clonipine
Lenox Gastaut - Minor Motor Seizures (Atonic or Myotic seizures)

 Atonic (Helmet kids: because have seizures that make them loose tone in body)
 Myotonic - have jerky movements
 Onset: 1 - 5 y.o.
 85% retarded
 EEG: slow waves & spikes < 3 cycles/sec ---------------------------------------------------- ***TQ
Absence (Petite Mal) seizures

 4 - 12 yo (never in anyone > 20 yo)
 Staring spells: 5 - 10 sec (look like dead with eyes open, this can be provoked by
hyperventilation)
 Positive family history
 EEG: 3 cycle spikes & waves/sec ------------------------------------------------------------- ***TQ
 No post ictal syndromes
 No Auras
 Prognosis is mostly good; usually kids outgrow it, better if no family history
 Rx: Ethosuccinoid & Valproic Acid ---------------------------------------------------------- ***TQ
Complex Partial (focal) seizure
 Affect the prefrontal area (Temporal lobe > Frontal lobe)
o Lowest seizure threshold high seizure incidence is found in hippocampus (short term
memory) because want it to fire easily. So any lesion or inflammation in temporal or
frontal lobes around hippocampus can cause seizures.
 Staring is seen but will perform complex motor activities during the seizure (ex. groom selves)
 Stereotypic behavior—repeated behavior ex. Can wipe of pants walk to the window and walk
back.
 Patients are never violent during these seizures
 Aura - occurs in complex seizures and migraine and is a sensation (smell) of something to
come. This will occur wherever the lesion is.
 There is post ictal confusion - patient doesn’t remember anything after
 Todd’s paralysis - transient, occurs as weakness after focal discharge in brain. Ex. arm after
the motor movement is patient with seizures will be weak after. Have to rule out infarction.
 Rx
o Carbamazepine (Tegretol), or Dilatin (Phenytoin) ------------------------------------- *** TQ
o Oxcarbamazepine (Trileptal): a new form of carbamazepine, or Gabapentin (Neurontin)
o Lobectomy if refractory
Grand mal (Tonic Clonic)

 Person gets rigid (Tonic) and than starts shaking (Clonic)
 1st tonic contraction followed by clonic jerking
o Generalized, Metabolic in origin (alcohol withdrawal) Phenobarbitol
 Rx:
o Phenobarbitol (Potassium or Sodium Bromide (KBr or NaBr))
o Carbamazepine (Tegretol) or Dilatin (Phenytoin)
Rolandic (ADNFLE) Epilepsy

 Autosomal Domminant Nocturnal Frontal Lobe Epilepsy
 Twitching of the face muscles during night
 Resolve by 13 yo in 85%
Status Eplapticus
 Life threatening (Emergency) due to failure to recover from SZ before another one begins.
 If SZ continues > 1 hour and if not stopped the brain will fry (Hypoxia  brain damage).
 Cause: Non-compliant patient with med or due to Metabolic derangements, infection, trauma
or misdiagnosis of the seizure type.
 Rx:
o ABC: Check airway and check heart if working  blood gases  O2  intubation
o Blood for Glucose, Electrolytes, CBC (Infection), BUN & ECG monitoring
o Thiamine - 100 mg. I.V. then 1 amp. (40 ml) 50% Dextrose and then Saline
 Remember: Always give Thiamine before Dextrose b/c a patient with alcohol will
develop Wernicke Korsakoff Encephalopathy (Thiamine Deficiency) ----------- ***TQ
 Also, don’t give Nitrous Oxide anesthesia for Vit B12 deficiency patients  severe
subacute combined degeneration (Post. Coll. & CS tract)  quadraplegia ------ ***TQ
o Drugs
 Benzodiazepines (Ativan - 0.1 mg/kg I.V. < 2mg/min) to disrupt seizure Then
give Dilantin (cant give more than 50mg.min or get QT elongation and give full
dose, can precipitate in dextrose solution so give saline) or Phosfenatoine (quicker
acting Dilantin)
 If seizures don’t stop give Phenobarbitol (will have to intubate since it will cause
stop breathing when given after Benzodiazepines).
Pediatric Seizures
Neonatal SZ
 1st day of life - due to hypoxia or hypoglycemia
 5-7 days - due to Hypo-Ca or narcotic withdrawal
 Later - due to infections or Metabolic derangement
 Rx:
o fix the cause
o Pyrodoxine & Phenobarbitol
 Prognosis is poor if sustained seizures or abnormal neurological symptoms are present
Febrile SZ
 Occur between 6 months & 5 y
 Duration < 15 minutes
 Febrile SZ will reoccur
 93% will never lead to epilepsy (7% may lead to epilepsy  25 y)
 Occur when a child has a sudden increase in temperature
 Will have a diagnosable infection
 If you never saw this patient before have to also think that it could be meningitis (H. Flu)
o Meningitis can produce a SZ so might need a lumbar puncture.
o In meningitis every minute is important to prevent long-term damage.
o If there is a family Hx of febrile SZ than might not have to do lumbar puncture.
 Rx: if > 3 febrile SZ  Phenobarbitol &/or Valium (suppository)
Atypical Febrile SZ
 Duration < 15 minutes
 Focal, not generalized
 Not with temperature swings
 Occur with clusters
 Abnormal Neuro Exam
 Need full evaluation
Other conditions arelated to seizures

 Toxemia in 2nd half of pregnancy
o Preclampsia & Clampsia (HBP + seizures: focal or Tonic-Clonic)
o Rx: Mg Sulfate
 PLEDS
o EEG pattern characterized by periodic complexes of sharp spikes with slow waves that
repeat every few seconds
o Due to cortical damage from hypoxemia (Encepholopathy), stroke or trauma.
o Not good prognosis
 7 - 17% of People with Generized Seizures Disorder may have sudden death (not due to seizures)
TRAUMA
Assessment & Evaluation of Head Trauma

 ABC (Airways, Breathing, Circulation)
 Every patient with Head injury has Cervical Spine injury until proven otherwise.
o C-spine X-ray (must see C7)
 Check surface of head, look at tympanic membrane (basilar skull Fx  CSF leak out from ear)
o Great risk of epilepsy if open head injury (50%), less if closed (10%)
o Closed Fx-temporal lobe epilepsy syndrome b/c it lies on skull and will scrape bone
 Assess level on consciousness (Glascow Coma Score)
 Check eyes (if one pupil is getting bigger they have a epidural Hematoma  emergency, must
be evacuated, and the increasing pupil size indicated increase pressure on third nerve.)
 Check reflexes, muscle strength, Babinski
 NO lumbar punctures with head injury to avoid Herniation
Rx:
 Monitor intracranial pressure (ICP)
o If ⇑ ICP use Hyperventilation, Manitol (osmotic diuretics)
 Surgery if Hematoma &/or open Fractures
Concussion & Contusion

 Transient loss of consciousness or other neurological function following Brain Injury
 No permanent neurological deficits following concussions
 Common problems with concussion (post concussive syndrome)
o Depression, dizziness (inner ear mechanism - otoliths used in acceleration and
deceleration, semicircular canals may be injured), migraine, stress, insomnia
 Post-traumatic Epilepsy may occur following brain contusions
Subdural Hematoma
 Surface or Bridging vessels torn from cerebrum
 Altered mental status
 Focal signs
 Headache
Epidural Hematoma
 Tear in Middle Meningial Artery
 Brief post traumatic loss of consciousness
 Lucid interval
 Ipsilateral papillary dilation
 Contralateral hemiparesis
Perinatal Trauma
 Types: Premature or Term
 Intraventricular Hemorrhage in Term infants can occur if there is difficulties during birth
 Premature Intraventricular - Periventricular hemorrhage
o If birth weight less 1500 gm there is a 40% chance that there will be bleeding into &/or
around their cerebral ventricles ------------------------------------------------------------ *** TQ
o SS: floppy with no muscle tones, agitated,
 ⇓ HR, ⇓ BP, ⇓ Hct, ⇓ To, ⇓ Respiratory Rate  Respiratory arrest
 Signs of ⇑ ICP with decerebration
o Grades ---------------------------------------------------------------------------------------- *** TQ
 Grade I: Intraventricular Hemorrhage just under ependymal ligning
 Grade II: Intraventricular Hemorrhage without dilation of ventricles
 Grade III: Intraventricular Hemorrhage with dilation of ventricles
 Grade IV: Intraventricular Hemorrhage with dilation of ventricles &
Intracerebral Hemorrhage (around the ventricles)
o Dx: Ultrasound on anterior fontanelle
o Rx: Supportive care and it may go away, keep child inside longer
C-Spine Burst Fractures

 When hit on top (vertex) of head, may have pressure transmitted throughout the cervical spine
and may have a burst fracture
 Seen in diving accidents
 Injury of C3, 4, 5  can have difficulty breathing
 Rx: Stabilize and fixate
Acute compression of Spinal Cord

 Medical Emergency
 SS:
o Neck or back pain
o Problem urinating (increase frequencies &/or incontinence)
o Defecation problems
o Weakness and numbness below lesion
o Retain feeling gradually if trauma is not so bad
 Dx: MRI
o If MRI is normal but neurological deficits are present  this is may be due to:
 Transverse myelitis
 X-Radiation myelopathy
 Arterial-venous malformations
 Rx -------------------------------------------------------------------------------------------------- *** TQ
o Give High Dose of Steroids (Methaprednisolone) to all patients with symptoms of SC
lesion (Reduce edema)
o X-Radiation Therapy to treat lymphoma
Anterior S/C artery occlusion syndrome ---------------------------------------------------------------- *** TQ
 Symptoms
o Loss of motor function & pain-temperature sensation below the level of the lesion
o Preserved posterior column function (position sense and vibration sense)
Brown Sequard (Hemisection of spinal cord) ------------------------------------------------------------- *** TQ
 Symptoms:
o Ipsilateral loss of motor function & proprioceptive sensory function
o Contralateral loss of pain-temperature sensation
Central cord Syndrome (Syringomyelia) ----------------------------------------------------------------- *** TQ
 Symptoms:
o Loss of motor, pain & To on both side
o * Mnemonic: MUD = Motor > Sensory; Upper > Lower; & Distal > Proximal
 Bilateral arm weakness > lower limb weakness with paresis more dense distally
than proximally
 Variable sensory impairment (pain & temperature sensory loss > propioceptive
sensory loss)
o Bladder dysfunction
COMA
Definitions
o Sleep - a state of non-pathological decreased mental status from which the patient can be
readily aroused to full consciousness
o Coma - refers to a state of markedly depressed consciousness such that the patient is
poorly responsive, or unresponsive, to vigorous physical stimuli
o Stupor - refers to a state of severely impaired arousal with some purposiveful
responsiveness to vigorous stimuli; however, the stuporous patient drifts immediately into
unconsciousness when vigorous stimulation ceases
o Obtundation - refers to a lesser state of decreased arousal with some purposiveful
responsiveness to touch or verbal stimuli
o Lethargy - refers to a state in which arousal, though diminished, is maintained
spontaneously or with repeated light stimuli; however, the lethargic patient often drifts
slowly into unconsciousness if left alone
o Confusion - refers to a state of adequate arousal, but with clinical evidence of cognitive
dysfunction
 Sudden onset of Coma can be due to: (Vascular or Traumatic)
o Cardiac  Hypoxia  Encephalopathy
o Subarachnoid hemorrhage
o Basilar (brainstem) artery occlusion
o Pontine hemorrhage
o Bilateral Cerebral infarction
o Brain Trauma
 Coma that developing minutes to hours can be due to: (Metabolic - Toxic)
o Metabolic – Hypoxic, Hypoglycemia, DKA, Renal, Hepatic
o Infection
o Toxic
o Hypertensive crises  Hypertensive Encephalopathy
o Reyes syndrome
 Focal deficits followed by Coma  Most likely due to Herniation
o Herniation can follow Brain Trauma, Hemorrhagic Stroke or Bleeding from Tumor
 Tonsilar Herniation  Medulla compression  stop breathing  Death
 Uncal Herniation  III nerve compression  pupil’s dilation
 Central (Thalamic) Herniation: Rare
*** It is often possible to differentiate metabolic coma from brainstem coma by methodically
evaluating brainstem function
 3 useful clinical indicators of brainstem dysfunction that can help differentiate Brainstem
coma from Metabolic coma:
o Abnormal breathing patterns
o Abnormal pupillary responses
o Abnormal eye movements
Management of Coma --------------------------------------------------------------------------------------- *** TQ

 ABC, IV, Foley Catheter, intubation if necessary
 * Give: Thiamine, Dextrose, Naloxone (narcotics antagonist), Flumazinil (Benzodiazepine
antagonists)
 ⇓ ICP: Hyperventilation  PCO2 < 25, Manitol: 1 g/kg IV over 10-30 minutes & Steroids
Diagram showing the change in pupil size and reactivity - depending on the site of pathology
Coma With Brain Stem Intact

 Can rule out reticular activating system
 Probably both hemispheres involved
 Normal CAT scan - could be metabolic, aneurysm rupture, or infection
o Need to Do lumbar puncture ------------------------------------------------------------- *** TQ
 Done when the intracranial pressure is NOT elevated
 Looking for infection or bleeding
 Abnormal CAT scan - divide into surgical or non-surgical
o Surgical:
 Subdural or Epidural hematoma
 Intracranial occupying lesion
Coma With Brain Stem NOT Intact

 If herniating  treat with hyperventilation to get the PCO2 to 25, then manitol, then
decatron (Hydrocortisone) ---------------------------------------------------------------------- *** TQ
 If not herniating  do the MRI again
 May have cerebellar or pontine hemorrhage
How to tell if brain stem is intact while in coma

 Do eyes move back and forth
 Need to rule out cervical spine fracture
 Ice water in ear (COWS)
 Put pressure on tempo-mandibular joint and then grimace symmetrically
 Blow on cornea and blink
Summary of some key clinical features of coma
 The combination of deep coma (even with total flaccidity or abnormal posturing) + briskly
reactive pupils almost always means a non-brainstem metabolic coma
 The combination of deep coma + spontaneous eye movements (or conjugate deviation of the
eyes on oculovestibular reflex caloric testing) almost always means a non-brainstem metabolic
coma
 The combination of coma + brisk pupillary reflexes + poor/absent eye movements strongly
suggests a sedative drug overdose
 A comfortable-looking patient, who has a normal breathing pattern +/- yawning, suggests a
metabolic coma
 An uncomfortable-looking patient + fixed mid-position/large pupil + absent eye movements +
abnormal breathing pattern +/- coughing/swallowing/hiccuping motions suggests brainstem
coma (primary or secondary) and the probable need for intubation and further aggressive
management
 The combination of DEEPENING coma + unilateral DILATING pupil (or an unilateral
dilated pupil not due to mydriatics or eye disease) suggests a rapidly expanding supratentorial
process and secondary transtentorial herniation until proved otherwise
 The DILATING pupil is usually on the side of the supratentorial pathology, while the
hemiplegia is usually contra-lateral (occasionally ipsilateral - suggests Kernohan's syndrome)
=> therefore use the dilating pupil as the primary guide when deciding on the likely side of
supatentorial pathology
VERTIGO / DIZZINESS
The most important initial determination that needs to be made in a patient with acute dizziness is to
determine whether the patient's dizziness represents True Vertigo - rather than being due to some other
specific/non-specific syndrome causing dizziness eg. non-specific lightheadeness or near-syncope/pre-
syncope or dysequilibrium syndrome
Spells - can be differentiated by History:

 TIA
 Seizures
 Syncope
 Migraine
 Psychiatric (panic attack)
 Transient Global Amnesia (no formation of any new memory for a short period of time)
 Periodic paralysis (due to K+ abnormalities)
 Vertigo
Focal Neuro signs & Spells occur in

 Migraine
 TIA
 Focal Seizures
Near syncope/pre-syncope: the sensation is that of "graying-out", lightheadedness, generalized

weakness, or a sudden overwhelming feeling that one is going to "pass-out"
Vertigo
 Sensation of disorientation in space with a sensation of motion where no motion exists, and the
sensation may be swaying, tilting or rotational in character:
o Mild vertigo may produce a feeling that the earth is moving or tilting slightly, or it may
produce a vague sensation of motion-sickness, or a feeling that one is being pulled to the
side; while severe vertigo may produce a distinct whirling sensation with prominent
autonomic symptoms of nausea and vomiting and sweating and pallor
o Vertigo is due to a mismatch of two-or-more of the vestibular, visual and proprioceptive
inputs to the vestibular system and thus any unilateral lesion of the vestibular apparatus
/ pathways may produce Vertigo
The distinction between Vertigo & Dizziness

 Vertigo: Illusionary sensation of turning of spinning either of the patients themselves or their
environment
 Dizziness: Lightheadedness, giddiness or feeling of uneasiness in the head
Must differentiate between acute peripheral vertigo (due to unilateral peripheral Vestibular disease)
from acute central vertigo (due to Cerebellar or Brainstem disease) ------------------------------- *** TQ
Causes of Peripheral Vertigo

 Middle ear disease
o May involve the labyrinth
 Meniere’s disease
o Vertigo
o Tinitis
o Deafness
 Benign Paroxysmal position Vertigo
o Epesotic vertigo
o Occurs with head turning or changing position
 Acute labyrinthitis
o Secondary to bacterial or viral infection
 Vestibular Neuritis
o Sudden attacks of vertigo & nausea with no auditory signs or symptoms
 Geniculate Ganglionitis
o Vertigo associated with ear pain & facial paralysis
 Post traumatic vertigo
o Possible damage to the labyrinth
Central Vertigo
 Vestibular nucleus is involved
o NOT the inner ear connections
o Commonly get Brainstem signs as well because the nucleus is near the MLF and other
cranial nerves involved in vision
 Can get Cerebellar symptoms
Central Vertigo patient will complain more about Balance problems & Nystagmus --------------- ***TQ
Peripheral Vertigo patient will complain more about Spinning ---------------------------------------- ***TQ
Central vs. Peripheral Vertigo
 Can distinguish by nystagmus
o Central vertigo - nystagmus usually worse towards the side of lesion
 Ex: right brain stem lesion, eyes jerk more when look to the right
o Peripheral vertigo - nystagmus usually worse (+2) when looking towards the good ear
Cataplexy (loss of muscle tone) ------------------------------------------------------------------------------ ***TQ

 Occurs in narcolepsy
 When falling asleep and getting up, have hallucinations and paralysis
 The only reason to give amphetamines other than with hyperactivity
 Need to rule out Lenotts Castow disease
 Antidepressants can help
Alcohol
 Mainly affect cerebellum (vermus)  ataxia
 Also affect the MD nucleus of Thalamus  problem in formations of new memories
o Must give Thiamine before Dextrose
 Wernicke’s encephalopathy ------------------------------------------------------------------ ***TQ
o Seen in chronic alcoholics
o Ataxia—affects vermis of cerebellum
 More trouble walking than with extremities
o Intranuclear ophthalmic lesions
 Strabismus of eyes (eyes look in different directions)
 Confusion
 Nystagmus
 Korsakoff’s Amnesia ---------------------------------------------------------------------------- ***TQ
o Also seen in chronic alcoholics
o Anterograde amnesia—loss of memory for things after amnesia started
o Can not form new memories
o Continues last for years
o Confabulations - if ask what have been doing lately they will make up stories because they
can’t remember
 Withdrawal seizures
o If heavy drinker who suddenly stops
 Auditory hallucinations with clear sensorium
 Delorium tremens=really bad shakes
• ~15% mortality
• Tremendous adrenergic rush
• High blood pressure, cardiac problems, heart attacks
• Rx: give them a sedative and then gradually withdraw them from that
o Typically Librium (Benzodiazepine)
Metabolic & other disorders that can produce toxicity
 Arsenic
o Get loss of muscle and weight
 Lead poisoning
o In children who eat paint
o ⇑ ICP, Coma & Seizures
 Reyes syndrome ---------------------------------------------------------------------------------- ***TQ
o Metabolic derangement post infection
o Upper respiratory infection that leads to liver derangement
o Vomiting, lethargy, liver function test decline (⇑ liver enzymes), sleepiness, ⇑ ICP 
eventually they herniated
 Hyperthyroidism -------------------------------------------------------------------------------- ***TQ
o Exopthalmos (bulging of eyes)
o Myopathy
o Worsens myasthenia gravis
o Hypocalcaemia periodic paralysis
o Atrial fibrillation
o Attention tremors
o Psychiatric disorders (Anxiety)
 Hypothyroidism ---------------------------------------------------------------------------------- ***TQ
o Muscle problems
o Peripheral Neuropathy
o Ataxia
o Diploplia
o Depression/Psychosis & Dementia
 Vit. B12 deficiency
o Don’t give Nitrous Oxide anesthesia for Vit B12 deficiency patients  severe subacute
combined degeneration (affect Posterior Columns & Cortico-Spinal tracts)  loss of
vibration with quadraplegia -------------------------------------------------------------- ***TQ
 Diabetes
o Nerve infarcts (III CN & other)
o More prone to strokes
 Ischemic strokes
• Especially if have hypertension
 Acute intermittent porphyria ------------------------------------------------------------------ ***TQ
o Metabolic problem with an enzyme involved in heme metabolism
o Inherited disorder
o Triad of symptoms
 GI
 Psychiatric
 Neurological
o Rx: high carb. diet then Indural prevents them from having the problem
NEURO – ONCOLOGY
 Metastatic Spread to Brain
o Most common are breast and lung cancer ----------------------------------------------- ***TQ
o Hypernephroma (kidney) and melanoma (skin) can also spread to brain
o Prostate cancer rarely metastasizes to brain
 Metastasizes to spinal cord & Posterior fossa via venous plexus (Batson plexus)
 Metastatic Spread to Spinal Cord
o Lung and breast cancer
o Prostate cancer  especially to lumbar area
o Lymphomas & Leukemia
  Spinal cord compression
 Acute - can give radiation even before scan because lymphoma is most common
and they are very radio sensitive (if cause unknown)
 Paraneoplastic Syndrome
o Cerebellar degeneration could be malignant
o Small cell cancer in the lungs  produces Eaton Lambert Syndrome -------------- ***TQ
 Small cell cancer can induce limbic encephalitis (rare)
 Antibodies against the presynaptic release of acetylcholine
 Myasthenia gravis is antibodies against the post-synaptic neuromuscular junction
 Eaton Lumbert is antibodies against the pre-synaptic release of Acetylcholine
• Have muscle weakness
o Eaton Lumbert gets better with exercise b/c more release of
acetylcholine
o Myasthenia Gravis gets worse with exercise
o Eaton Lumbert does NOT usually involve the face
o Myasthenia gravis does usually involve the face
• Eaton Lumbert get dyploplia
o Sensory neuropathies
 Lose sensation in legs unexplainably
 Can come from cancer (from somewhere else)
 Dementia
 Obstoclonus/Myoclonus ----------------------------------------------------------- ***TQ
• Commonly seen with neuroblastoma
• Myoclonus - jerking movements of any part of body
• Obstoclonus - jerking movements of the eyes
o Progressive Multifocal Leukoencephalopathy ------------------------------------------- ***TQ
 Due to papovo virus when immunosuppressant
 Can also get DIC (disseminated intravascular coagulation) emboli infarction
o Shingles from herpes zoster
 Pain  Vesicular rash
 Common in immunosuppressed who get cancer
 Leukemia & lymphomas
o Leukemia can affect the CNS in that:
 If affecting platelets  get bleeding
 If affecting WBCs  get infections (ie. meningitis)
 Leukemic cells can get into the CNS  Carcinomitis meningitis
• Very high protein levels and very low glucose levels in CSF
 Lymphoma can also produce spinal cord compression
1˚ BRAIN TUMORS
 What to know
° Posterior fossa tumors
° Spinal cord tumors
 POSTERIOR FOSSA TUMORS (MECAG) ----------------------------------------------- ***TQ
° Cereberallar Astrocytoma
 Location: In cerebellar hemispheres
 Clinical: Ataxia in ipislateral extremities (arm or leg on same side)
 Prognosis: Excellent with surgical therapy
 Timing: Symptoms takes months to develop
 Typical pt: Older child
° Medulla Blastoma
 Location: Along the midline of the cerebellum
 Prognosis: Good with chemotherapy
 Timing: Symptoms develop quickly
 Pt: Youngest children
° Ependymoma
 Location: Around lining of the 4th ventricle
 Timing: Symptoms develop quickly
° Brainstem Glioma
 Location: Within post fossa, in the brainstem
 Prognosis: Worst prognosis, no treatment
° General Characteristics
th
 Can ⇑ ICP b/c of impeded flow through 4 ventricle
 Esp. Medulla Blastoma, Ependymoma (b/c they are more midline)
 Youngest kid/shortest duration → Oldest kid/longest duration ----------- ***TQ
 MB → Ep → CA → BG (MECAG)
 Greastest chance of survival → Worst Prognosis --------------------------- ***TQ
 CA → MB → Ep → BG
 MIDLINE CERBERAL TUMORS
° In 3rd ventricle
 Colloid cyst
 Obstructs fluid
 Choroids Plexus Papilloma
 In choroid plexus
 Ependymoma
rd
 In ependymal lining of 3 ventricle
° Pineal (around 3rd ventricle)
 Gliomas
 In hypothalamus/thalamus
 Clinical: Intense muscle wasting syndrome
 Teratomas
 Dystreminomas
 Pineolma
 Clinical: Early sexual development
 Neuroectodermoma
 OPTIC PATHWAY TUMORS
OPTIC NERVE TUMORS ----------------------------------------------------------- ***TQ
°
 No vision problems: Benign enlargement of optic nerve
 Vision problems: Meningioma or Glioma
° OPTIC PATHWAY TUMORS (nerve+chiasm) ----------------------------------- ***TQ
 Neurofibromatosis
 Type of optic nerve Glioma
 Clinical
• Lesions on skin
• Neurofibroma tumors around peripheral nerves in PNS
• Brainstem & Optic nerve gliomas
 Rx: Radiotherapy (only after the age of 7 years)
 SUPRASELLAR & CHIASMATIC
° Craniopharyngiomas
 Diabetes Insipidus develops after surgery
 ⇓ Vasopressin (compound released from post pituitary)
 ⇑ Urination
 Treatment: Vasopressin
 HEMISPHERIC CEREBRAL
° Intraventricular
 Ependymomas
 Choroid Plexus Papillomas
° Parenchymal
 Glioma
 Most common cancer in Brain Parynchyma
 Has different stages
 Oligodendroglioma
 Meningioma
 Neuroectodermal
° Glioblastoma Multiforme
 Stage IV of Glioma
 Most malignant
° Glioblastoma Cerebri
 Glioma diffuses in neurons
 Spreads throughout brain
 Very deadly
SPINAL CORD TUMORS ---------------------------------------------------------------------------------- ***TQ

 INTRAMEDULLARY (15%)
° Location: In spinal cord
° Types:
 Ependymoma ------------------------------------------------------------------- ***TQ
 Most common (65%)
 Note:
• Cyst of the central canal in cervical lesion = Syringomyelia
• & if it is in the brain stem = Syringopolvia
 Astrocytoma/glioma
 Because these are the supporting cells
 More rare (35%)
 EXTRAMEDULLARY INTRADURAL (60%)
Location:
° Outside of spinal cord, but within the dura
Types
°
 Menengioma
 Occur in middle age females
 In thoracic spine
 Neurofibromas
 Anywhere in spine
 Dumbell Neuromas
• Go through dura, then come out
• Dumbell in shape
 EXTRAMEDULLARY (25%)
° Location: Outside of spinal cord and the dura
° Types
 Herniated disc
 Metastasis
 Lymphoma
 Arteriovenous malformations (can be intra/extra)
 Fractures
 Dislocations
 Abscesses
 Note regarding the MRI
° When people have back pain they get an MRI
 50% lumbar MRI
 50% cervical MRI
 Nobody gets thoracic MRI
° Be careful!
 Rare herniated discs can occur in that region
 Women can have a Benign Menengioma in the thoracic (a benign tumor that
can easily be removed and cure all symptoms)
 Men can have AVM that can present as a tumor
° Thoracic spinal cord symptoms ------------------------------------------------------ ***TQ
 ⇑ Reflexes in Legs, ⇓ reflexes in arms
OTHER SPINAL CORD LESIONS
 CONUS MEDULLARIS
° L2 on adults (lower on children)
° Area of origination for all L2 and lower nerves: pelvic, genital, lower extremities
° 1/2 inch long → tiny but controls a lot, tumors here are very BAD
° Lesion in this (L2-L3) level causes
 Saddle anesthesia (in between the legs)
 L2, 3, 4: knee jerk lost
 S1: ankle jerk lost
 Sex and urinary bladder dysfunction
 ⇓ Anal sphincter tone
 CAUDA EQUINA
° Fibers below conus medullaris
° Lesion causes (similar to “pinched nerve”)
 Unilateral symptoms
 Variable deep tendon reflexes
 SPINAL DISC HERNIATIONS
Most common: L5-S1
°
Next most common:
° L4-5
Rare: ** Central herniation of disc at L1-2, L2-3 levels  will effect Conus
°
Medullaris
 VASCULAR VS. NEUROGENIC CLAUDICATION ----------------------------------- ***TQ
° Vascular Claudication
 Pain after periods of activity (It’s like having angina pectorus in you legs)
 Atherosclerosis of the legs, not enough blood getting to legs
 The more you use the muscle, the more it hurts
 Clinical (Pain with Exercise)
 Pain ⇓ when relaxing, and ⇑ during activity
 ⇓ Pulses in feet, and medial malleosis
 Hair growth in feet area
 Treatment: bypass surgery to bring blood to legs
° Neurogenic Claudication
 Due to Lumbar Stenosis
 Clinical (Pain with Standing)
 Bulging discs
 Arthritis
 Osteocytes
 Tight region between L3, 4, 5 (cauda equina region)
 Pain (Positive Line or Curb Sign)
• ⇑ w/Standing or extending the neck (closes spaces where nerves
exit)
• ⇓ w/Sitting down or flexing the head forward
========================================================================
CNS INFECTIONS
Meningitis
 ACUTE ASEPTIC
o Nonbacterial Meningitis, or inflammation of the subarachnoid space, generally viral
usually self-limited and results in a lymphocytic pleocytosis
o Clinically, less fulminant than bacterial meningitis
o Causes:
 Viral: Echovirus, nonparalytic poliovirus & coxsackievirus, etc.
 Low pathogen Bacteria: Staph Albus, Lyme, Listeria, syphilis, Q-fever
 Non inflammatory causes:
• Subarachnoid hemorrhage
• SLE & RA
• Carcinomatous meningitis
o Aseptic Meningitis: ⇑ lymphocytes, ⇑ protein, normal glucose ---------------- TQ
o Carcinomatous Meningitis: ⇑ lymphocytes, ⇑⇑ protein, ⇓⇓ glucose ----------- TQ
 ACUTE SEPTIC / BACTERIAL
o Life threatening (Neurological emergency)
o Pathology: Bacterial inflaming  edema & destruction of the cerebral cortex  seizures,
confusion or focal neurological signs.
o CSF: ⇑ poly (Not lymphocytes), ⇑ protein, ⇓ glucose
o Other CSF tests:
 Gram Stain: (not accurate test): 10% false negative, 30% false negative
 Counter immuno electrophoresis (CIE) is very accurate:
• 90% -accuracy with H. flu, B. strep & meningococcus
• 50% accuracy with pneumococcus
 Limulus Lipate / (horseshoe crab test): 90% accuracy for Gm-ve bacteria
 India Ink: Cryptococcus
 Acid-East: TB
 Anaerobic: Cultures (specially base skull fracture & Alcoholics)
Most causative organism according to age

BE-HNP
Neonate ( < 2 months) E. Coli & Group B Strept • 10 –30 % mortality
• Rx: Amp. & III generation Cephalosporine
• Unknown: Amp. & Aminoglycosides (Gynt)
Infants H. Influenza • Basilar exudates
• Rx: Amp. & Chloromphynicol
o Vancomycine & III generation Cephalosporine
Teens/ young adults N. meningitidis • Cortex
• Waterhouse Fridrickson Syndrome: Rash &
adrenal collapse associated w/meningitis
• Rx: Pen. or Amp. & Ceftraxone
Elderly Pneumococcus Cortex
 Staph, Strep epidermitis

• Intraoperative contamination: due to shunt placement b/c of normal pressure
hydrocephalus
 Niglaria
• Ameba: Lives in fresh water ponds
 Leptospirosis & Lymphocytic Chorionic Meningitis (LCM)
• Rodent exposure
 Cryptococcus: Pigeons
 Coccydium: Seen in south-western U.S.
 Strep Pneumonia: Alcoholics can get pneumonia and meningitis
 CHRONIC MENINGITIS
 CSF: ⇑ lymphocytes, ⇑ protein, Normal or ⇓ glucose
 TB Meningitis
• Pt gets lung TB  Brain
• Thick exudate bathes the base of the brain
• Cranial nerve (esp. CN7 & CN6) signs develop & Dementia
 Syphilitic meningitis
• Produces dementia
 Cryptococcus
• Occurs mostly in HIV pts (prophylaxis taken)
• India Ink
 Coccydium mycosis
• Sewankeen Valley fever
• Common in south-west US
 Fungus
• Symptoms: cold, headache, fever, cough, myalgia, apathy, confusion
COMPLICATIONS of Bacterial Meningitis - Neurological Sequele

o Abscess formation  evacuation
o Subdural empyemal effusion (pus)
o Hydrocephalus (if exudates blocks ventricle in TB meningitis)
o Infarcts and necrosis of cortex
o Epilepsy (with seizure formation from scar tissue in cortex)
o Deafness (b/c of temporal lobe, mastoid, or inner ear problems)
o Mental retardation
o Death
BRAIN ABCESSES
 Most common place: Frontal lobes (b/c they have the most surface area and mass) then temporal,
parietal, occipital
 Symptoms: headaches, neurological signs, fever
 Most common cause: anaerobic infection
o Other causes: Trauma, neurosurgical manipulation, infection of nearby sinus, blood spread
from heart or lungs
 Dx & Rx: LP if safe, drainage & Antibiotics (Pen. or Amp. & Chloromphynicol)
ENCEPHALITIS
 Encephalitis vs. Meningeal Encephalitis
o Encephalitis: refers to brain infection, like Herpes Simplex Encephalitis (HSE)
o Menengial Encephalitis: refers to inflammation of meniges
 HERPES SIMPLEX ENCEPHALITIS (HSE) --------------------------------------------------------- *** TQ
o Most common brain infection
o Presents with focal symptoms & targets mainly Neonatal
 HSE type II at birth
• 60 % mortality if fetus gets Herpes Simplex Encephalitis
• Cause vesicular rash, conjunctivitis, jaundice, bleeding, seizures & coma
• A woman with genital herpes MUST give birth via c-section!
 Adult form of HSE
• AKA Limbic Encephalitis (b/c it affects the limbic system)
o S & S ------------------------------------------------------------------------------------------ *** TQ
 Before it enters the brain: Genital herpes, bells palsy, vesicular rash
 Once it enters the brain: Bizarre behavior initially, then high fever, lethargy,
Seizures, Confusion  Coma  Death
 CSF: ⇑ Polys, ⇑ Protein & RBCs
o Target & Dx
 Frontal region & Temporal lobes (maybe b/c it enters through sinus)
 MRI shows temporal lobe gets inflamed & necrotic
 Encephalogram shows spike activity in temporal lobes
o Rx ----------------------------------------------------------------------------------------------- *** TQ
 Treatment must be started at earliest suspicion
 Pts with meningitis start treatment with a Acyclovir (IV) while waiting for results
o Oat-cell Cancer
 Paraneoplastic syndrome --------------------------------------------------------- *** TQ
 Symptoms resemble Herpes Simplex Encephalitis (Limbic Encephalitis)
 SYPHYLIS
o Great Mimicker (along with HIV) b/c there is a great variety of possible symptoms
o Sx & Dx
 May be Asymptomatic, just involve genitals & joints
 CSF for VDRL even if blood VDRL is negative
 CSF: ⇑ lymphocytes, ⇑ protein, Normal glucose
 Syphilis meningitis with cranial nerve palsy & epilepsy
 Inflammation of arteries & Strokes
 General Pareisis: Dementia w/Upper motor neuron lesions
 Argyle-Robinson pupils ---------------------------------------------------------- *** TQ
• Accommodate (far to near), but don’t react to light
• Prostitute Pupils: with syphilis would Accommodate, but Not React
 Optic Atrophy with blindness
 Diffness
 Dementia
 Tabes-Dorsalis: ⇓ vibration, ⇓ proprioception, ataxia  (+ Romberg sign) &
+ Babinskis ---------------------------------------------------- *** TQ
 Anterior spinal syndrome: infarct  damage to corticospinal tract ⇓ pain
 HIV
o Neurological Symptoms
 Dementia
• Deficits in attention & concentration
• Due to demyelination between frontal lobes & the rest of the brain
 Myelopathy
• Due to demyelination of spinal cord
 Myopathy
• The muscle are affected  proximal weakness
 Neuropathy
• Can affect axons or myelin around nerves
• Can affect the blood supply  Infarction of nerves
 Opportunistic infections .
• Toxoplasmosis meningitis
• Cryptococcal meningitis
 Neoplasms
• Lymphoma
• Leukemic infiltration
• Plasmocytomas
• Karposi’s sarcoma (which can go to brain)
 Vascular
• Ischemic or hemmoragic vascular abnormalities
• Due to arteritis & maybe associate with syphilis
 Parasites
o TOXOPLASMOSIS
 Pigeon exposure
 Common in HIV
 Sx & Dx
• MRI or CT scan w/contrast
o Ring Enhancing Lesions (Hole with surrounding inflammation)
• CSF: ⇑ Lymphocytes (Eosinophylia), ⇑ Protein & ⇓ glucose
o Remember: ⇑ Lymphocytes in Viruses, Fungus & Parasites
⇑ PMN in Bacteria
o CYSTICEROSIS
 Tinea Solium (uncooked pork)
 Most common parasitic infection of the brain world wide
 Ova in GI  travel to blood as oncoshperes  travel to brain  lodge into small
blood vessels  live for 1-2 years w/out problems  they die  the area where
they died becomes inflamed  damage occurs corresponding to that area
 S & S (depend on location)
• Ex. bugger dies in Right Cerebellar Hemisphere  Ipisilateral ataxia
• Ex. Lenticulostriate arteries on the left  contralateral paralysis
• Can spill out into 3rd ventricle (must be scooped out during surgery)
 Rx: Steroids, Prasiquantal, Albendazole, etc
 Viruses
o HERPES ZOSTER - SHINGLES
 Occur in 50-70 y.o.
 S&S
• Severe Dermatome Pain BEFORE Rash ----------------------------- *** TQ
• Usually in thorax dermatomes, but could be a cranial nerve, too
• Papullo-vesecular rash followed by resolution of the rash
• Severe post herpatic pain may continue for long time
 Rx
• Steroids
• Acyclovir or Fanvir
• Pain management (Antidepressants & Narcotics if needed)
o CYTOMEGALOVIRUS (CMV)
 Causes multifocal lesions in the brain
 Occurs in immunosurpressed pts (Iike cancer or HIV pts)
o PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (PML)
 Papovavirus
 Occurs in immunosurpressed pts (Iike cancer or HIV pts)
DEMYELINATION OF CNS & PNS
I. CENTERAL NS DEMYELINATION
° Primary Idiopathic disease
 Multiple Sclerosis **
 Most common cause of Central NS Demyelination
 Devic’s Disease
 Variant of MS
 Transverse myelitis: inflammation of one segment of the sp cord
 Optic Neuritis: inflammation of optic nerve
 Schilder’s Disease
 Adrenoleukodytrophy
 X-linked Recessive
 “lorenzo’s oil” disease
 Balo’s Disease
 Variant of Schilder’s disease, but with more cysts
° Infections or vaccines which illicit demyelination
 Papova virus
 Cause progressive multifocal leukoencephalopathy in Immuno-
compromised pts?
 MMR (measles/mumps/rubella) & Epstein Barr & Varicella
 Cause demeylination
 Rubeola virus
  Causes SSPE (Subacute Sclerosis Pan Encephalitis)
 Very similar to Jacob-Krutzfield disease (Mad Cow Disease)
° Nutritional
 Rapid correction of hyponitremia with saline --------------------------- ***TQ
  Causes CPM (Central Pontine Meylinolysis)
 Pons becomes demyelinated
 Toxins in home-made wines
 Marchiafava Bignami syndrome
° Inherited
 Causes everything (neuropathies, myopathies)
° Toxic/Metabolic
 Radiation
  Melts myelin
 Alcoholism
  Hurts myelin (esp. in vermis area of cerebellum)
 B12 deficiency
 CO poisoning
 Hypoxia (⇓ O2)
 Mehothrexate (chemotherapy agent)
° MULTIPLE SCLEROSIS ------------------------------------------------------------- ***TQ
 Diagnosis
 ** There must be two different lesions separated in time and space
 Optic neuritis or one episode of Transverse Myelitis ≠ MS
• Neuro exam
• MRI (see areas of demyelination in spinal cord &/or brain)
 Myelin basic protein in CSF
• Because it is being broken down
 Oligoclonoal band in CSF
• Evidence of antibody reaction against protein
 ⇓ speed of Evoke Response
• ⇓ Visual ER: Measures how fast electrical activity goes from retina
 Optic n.
• ⇓ Auditory ER: speed from tympanic membrane → auditory
cortex
• ⇓ Somatosensory ER: speed from skin → somatosensory cortex
 Prognosis, variable: some pts…
 Have only two episodes their whole lives
 Keep getting progressively worse
 Cause (most probable!!!)
 Viral presentation, maybe Corona Virus
 Body reacts to virus
 Body cross reacts the antibody response to CENTRAL myelin
 Geographic
 More common in temper climate, less in tropical
 Maybe viral exposure in EARLY LIFE causes MS b/c
• Moving at 17 from Costa Rica to NY → ⇓ risk
• Moving at 17 from NY to Costa Rica → ⇑ risk
II. PERIPHERAL NS DEMYELINATION

 GUILLIAN-BARRE ------------ {GEIAN BERE’} -------------------- *** TQ
o Most common cause of Peripheral NS Demyelination
o Prognosis: If recognized early, pt can be saved, if not pt dies!!
o Cause
 Upper respiratory infection due to virus
 Body develops antibodies and cross reacts to PERIPHERAL
myelin
o Symptoms
 Ascending paralysis: Weakness starts in legs & goes up
 Lost deep tendon reflexes
 Pin prick sensation is spared, vibration in lost
o Diagnosis
 ⇓ Nerve conduction velocity test (measure speed of impulse)
• Decreased, especially when directed towards the spinal
cord and back, as in deep tendon reflex
o Treatment
 Steroids
 Plasmaphoresis: filters antibodies against the myelin
 Chemotherapy
 CHRONIC RELAPSING IDIOPATHIC POLYNEUROPATHY (CRIP)
o Chronic form of Guillian-Barre
o Chronic progressive demeylination of PNS
o Pts: Usually occurs in older men
o Symptoms: More sensory loss than Guillian-Barre
o Treatment: Steroids
 MILLER-FISCHER variant of Guillian-Barre
o Symptoms
 Paralysis of ocular muscles
 Ataxia of limbs
 ⇓ Deep tendon reflexes
o Cause: upper respiratory infection
o Progressive
========================================================================
Peripheral Neuropathy / Neuromuscular Junction
Muscle Weakness
 Weakness in proximal part of the leg or the shoulder. That typically refers to Myopathy.
 Exceptions such as Guillian Barre & Werdnig-Hoffman neuropathies can sometimes give
proximal weakness.
 In general: ---------------------------------------------------------------------------------------------- *** TQ
o Myopathy gives Proximal Weakness
o Neuropathy gives Distal Weakness
Muscular Dystrophies
 Duchenne-Becker Dystrophy ---------------------------------------------------------------------- *** TQ

o Replacement of muscle tissue with fatty tissue
o Decreased muscle strength & reflexes
o Proximal muscle weakness in the Flexor mm
o Children < 5 years of age are struck by having difficulty with walking
 When the child is placed on their butt sitting on the floor, they will actually climb
on their own legs to get to a standing position. (Gower’s sign)
 There is a slight improvement when they grow until 8 y, then they have more
problems walking and weakness.
 Usually by 9-10 yrs of age they end up in a wheelchair.
o Genetic problem:
 Dystrophin deficiency  muscle membrane damage  death of the cell
 Women are carriers & Men get the disease.
o Varients:
 Duchenne is the Dystrophy
 Becker variant is more mild form: The onset is > 5 y.o. & children walk longer.
o Dx
 CPK (Creatine phosphokinase) is the characteristic blood test for Duchenne
Dystrophy --------------------------------------------------------------------------- *** TQ
• CPK-MM - ⇑ in skeletal muscle damage (Duchenne disease)
• CPK-MB - ⇑ in heart muscle damage
• CPK-BB - ⇑ in brain damage (rarely used)
 EMG has a myopathic pattern
• There is a problem with the motor unit of the muscle
o The motor unit is smaller in myopathy
o The motor unit is bigger in neuropathy
Fascio-Scapulo-Humural (FSH) Dystrophy .

o Facial, scapular and humural muscles become weak and atrophies
o They have some ⇑ in CPK
Limb-Girdle Dystrophy
o Progressive weakness of a limb-girdle
o Inherited
VonFuch’s Disorder
o Affects eye muscles: (Occulopharyngeal) Dystrophy
o Effects eye muscles and the pharynx giving you problems with swallowing.
Myotonic Dystrophy ------------------------------------------------------------------------------------------ *** TQ

o Myotonia refers to the phenomena of muscle contraction but the problem with relaxation
o Must rule out metabolic disorders, thyroid, or inflammation of muscles, which can make
them difficult to contract (polymyocitis) or potassium problems (periodic paralysis)
o Classic disorder is Myotonic Dystrophy also known as Steinart’s Disease
 The weakness is distal in this disorder ------------------------------------------- *** TQ
 These people have frontal bolding, Temporalis muscle (temporal) wasting. They
have cataract, adrenal insufficiency, diabetes, gonadal atrophy, and heart problem
 EMG will have a pattern called dive-bomber pattern
• There is an increase frequency discharge & you will hear a sound
• These pattern are heard in myotonia
Myotonia congenita (Thomson’s Disease) ---------------------------------------------------------------- *** TQ

o Characteristic is myotonia
 Myotonia makes muscle very big but these people can’t move very fast.
 People with this disorder have Herculean appearance even though they are weak
and slow because they can’t relax their muscles
 To remember these disorders associate it with strongmen in circus
Paramyotonia congenital
o Affects face forms & hands
Schwartz
o Cranial myotonia in infants
o Abnormalities of the skeletal systems
Congenital myotonia
o Children of mothers with myotonic dystrophy can have respiratory failure and
myotonic weakness at birth.
Inflammatory Myopathies .
o Refers to inflammation of muscles
o Polymyositis & Dermatomyositis
Poymyositis --------------------------------------------------------------------------------------------------- *** TQ
o Weakness
o No family history
o > 30 years onset
o ⇑ CPK
o Don’t have rashes or any nerve problems
o No other causes of muscle inflammation from alcohol, drugs, or thyroid that would cause
inflammation
o Autoimmune disorder - altered cellular immune response. Lymphocytes are
synthesized against muscle cells and cause inflammation
o Extra ocular muscles are spared
o Rx: Steroids
Dermatomyositis ---------------------------------------------------------------------------------------------- *** TQ

o The same muscles are attacked but there is different pathology
o They have antibodies against muscle cells
o Rashes are in lupus-like facial area (around the eyes and cheekbones)
o Usually occurs in younger people
o Malignancies have to be ruled out when this disease occurs in adults.
o Rx: Steroids
Polymyalgia Rheumatica
o Muscle inflammation
o A lot of women (greater than 55) with aches and pains
o Much more common disorder where steroids are also helpful
o May be associated with temporal arteritis (inflammation of the arteries and can get infarcts
of the optic nerve-ischemic optic neuropathy)  Increased sedimentation rate
Inclusion body Myositis - (all you need to know is the name)

 Congenital Myopathies
o Central core, myotubular, or central nuclear
o Present at birth
o Need to be ruled out in children who are born floppy
o Muscle biopsy if nothing else can be figured out
o EM-see the pattern
 Werdnig-Hoffman ----------------------------------------------------------------------------------- *** TQ
o Involves anterior horn cell but produces proximal weakness (although, it is Neuropathy)
o Baby will not kick as much in utero  will be born with lively eye movement but they will
be floppy. Can look like ALS Fasciculation in their tongue because anterior horn cell are
dying and the muscles are not being innervated properly.
o They usually die by three years of age
o There are variants of this disorder.
 Kugelber-Welander --------------------------------------------------------------- *** TQ
• Much more benign variant of Werdnig-Hoffman
• The onset is not until children are 5-15 years old and they have some
muscle weakness
o Werdnig-Hoffman can be distinguished from ALS based on muscle biopsy & progression
 ALS has rapid progression and it involves Anterior Horn & Corticospinal Tract
 Werdnig-Hoffman has gradual progression ------------------------------------ *** TQ
Periodic Paralysis
 Periodic acute episodes of weakness due to potassium abnormalities. These can be congenital
 Hypokalemic & Hyperkalemic forms of Periodic Paralysis
o HYPOKALEMIA
 Predominantly in males in their twenties and if they have a lot of exercise & eat a
lot of carbs  glucose & potassium will get into the cells and they will get these
attacks of weakness
• Kid’s playing football has some pizza, and they can’t or have difficulties
moving the next morning.
 Patients can get respiratory paralysis but it is really rare.
 Rx: supplements of Potasium
o HYPERKALEMIA
 More rare and occurs in both males and females in 7-20 years of age.
 It is less severe and they can have some myotonia associated with it.
 Rx: bring potassium down by giving Diuretics (Lasix, Diazide)
Carnitine Deficiency
o Carnitine carries long chain fatty acids inside the mitochondria.
o This deficiency leads to all kinds of muscle & liver problems.
o Can look like Reyes syndrome with increased intracranial pressure, in addition to swelling
of the brain and liver problems
o These are typically inherited
Kearns Sayre Daroff

o Type of carnitine deficiency with mitochondria problems
o Muscle weakness
o Onset is less than 20 years of age
o Children have weakness in their eyes with retinal degeneration
o They can also have heart problems and ataxia
Mitochondrial Encephalopathy
o Problems with mitochondria in the brain
o Brain cells have ragged red fibers in mitochondria
o Cytochrome oxidase complex 4 defect
Mitochondrial encephalopathy with Lactic Acidosis and Strokes (MELAS)

o Can cause stroke in young adults.
o Complex one deficiency
NERVE DISORDERS
Nerve Disorders
 Neuronapathy: disease of the Nerve cell body
 Axonapathy: disease of the Axon
 Myelinopathy: disease of the Myelin
o Most important myelinopathy is Guillian-Barre
 Axonapathy
o Most common type of neuronapathy
o Occur in patients with diabetes & uremia
 Axons start dying because of other metabolic disease
o Glove & Stocking sensory & motor loss: and they can have early symmetrical loss of the
ankle jerk and moderate slowing of the nerve conduction velocity. If the myelin is lost
nerve conduction is slowed
 Neuronopathy
o anything that hits the nerve cell body (anterior horn cell)
o Werdnig-Hoffman & ALS - syndromes are involved in neuronopathy
Nerves can be affected by ischemia

o In diabetes  pupil sparing III nerve palsy
o Diabetes can also  infarct of lateral femoral cutaneous nerve  Acute pain in the thigh
o Diabetics, in general, are more sensitive to nerve infarcts & nerve compressions
Nerve compression in the Upper Extremities

o Ulnar nerve behind the elbow  Cubital tunnel syndrome – Most common symptom
of compression of the peripheral nerves
o Median nerve in the wrist  Carpal tunnel syndrome
o Median nerve under pronator teres  Pronator teres syndrome
o Radial nerve that wraps around the humurus  Bridegroom palsy
o Damage of the Radial nerve  wrist drop & weakness in the arm
o Damage of the Ulnar nerve  Claw hand : (increased flexion of the fourth & fifth digits)
Nerve compression in the Lower Extremities

o The most common sites of nerve compression in the lower extremity:
 Peronial Nerve (behind the fibular head)
 Tibial Nerve (in the dorsum of the foot
Hereditary Sensory Motor Neuropathy (Type I, II, III & IV)

 Charcot-Marie-Tooth (CMT) Disorder ----------------------------------------------------------- *** TQ
o This is the inverted champagne bottle legs/the stork leg deformity
o distal muscles below the knees become atrophied.
o  Peronial muscle atrophy and it is a demyelination problem
o There is a milder form of this disorder. It is called a neuronal form
 Dejerene Sotto (Type III) ---------------------------------------------------------------------------- *** TQ
o Onion bulb formation on the nerves
o Onion bulbs refer to the fact that there is demyelination & remyelination
 Repsum disease
o Refers to deficiency in phytanic acid and they get some neuropathies and it is hereditary.
Neuro-Muscular junction disorders (Myasthenia Gravis) -------------------------------------------- *** TQ

 Autoimmune disorder
 Antibodies are made against neuromuscular junction
 Involve the cranial nerves & brainstem (ocular, bulbar groups of myasthenia gravis)
 Usually seen in young females & older males
o Young females have good prognosis because antibodies seem to come from thymus gland
 if you remove thymus glad, the patient is cured.
 This is even with the hypertrophy of the thymus gland and not with Thymoma
o Acute severe Myasthenia Gravis occur in older men
  Respiratory complications
 S&S
o Fatigability
o Ptosis & Pharyngeal problem (problem swallowing)
 Dx
o Blood test for anti-ACH-receptor antibodies or striated muscle antibody or extra-
juctional receptor antibody
o Tensilon Test
 Tensilon inhibit Acetyl Cholinesterase (⇓ breakdown of Ach)  ⇑ Ach in the
Neuro-Muscular junction
 The patient is given Tensilon  patients rapidly get better
o EMG shows the decrement response to three cycles per second stimulation ----*** TQ
 Remember in EEG: Three cycle per second is seen in Epilepsy (Petite-Mall)
How to difference between Myasthenic crisis & Cholinergic crisis? -------------------------------- *** TQ
 Cholinergic Crisis
o ⇑⇑ Ach
o Parasympathetic system is involved because Ach is the neurotransmitter of this system
o  Slow heart rate
o  Abdominal cramping (due to ⇑ blood flows to the intestine)
 Myasthenic Crisis
o ⇓⇓ Ach
o  Weakness
 If the patient takes too much Mestinon or Tensilon  ⇑⇑ Ach  cholinergic crisis
 If they have ⇓⇓ Ach  myasthenic crisis
EMG
 Insertional activity: When the patient is relaxed & not moving there should be no muscle activity
o If there is a negative deflection it is called a positive sharp wave
o If there is a positive deflection it is called fibrillations
o Fibrillations & positive sharp waves are signs of nerve problems (Not muscle problems)
o . (polimysitis: characterestc EMG pattern)
 Motor unit potentials:
o LMN disease  large motor unit potentials
o Myopathic disease  small motor unit potentials
 Typical EMG patterns in Neuropathy
o Large motor unit
o Fibrillation is in positive sharp waves
o Increased interference pattern
 Typical EMG patterns in Myopathy
o No spontaneous activity or small motor unit potential
o Normal insertional activity
 EMG pattern of Pyomyositis ---------------------------------------------------------------------- *** TQ
o Inflammation of the muscle but the muscle is also dying
o  Combination of both Myopathy & Neuropathy patterns
o Muscular dystrophy with pinched nerve in the back  give the same pattern as Pyomyositis
PEDIATRIC NEUROLOGY
Floppy baby is born - where is the lesion?

 The lesion can be in the brain (encephalopathy or inflammation of the brain), anterior horn cell, or
the spinal cord transection, or maldevelopment of the spinal cord, Werding-Hoffman disease,
peripheral nerve disease, MNJ disease, muscle disease, or the systemic cause.
Most important Diseases in Pediatric Neurology

 Acute ataxia in childhood
o Problem with the cerebellum (tumor, inflammation, toxin exposure)
o Neuroblastoma can give Acute Ataxia with Myoclonic Jerks & Opsoconis (abnormal
movements of the eyes) ---------------------------------------------------------------------- *** TQ
 Mample syrup urine disease .

o Problem with branched chain amino acids  Acute Ataxia
 Hartnup Disease -------------------------------------------------------------------------------------- *** TQ

o Problem with tryptophan metabolism : decreased absorption
o Acute Ataxia
o Bizarre behavior
o Light sensitivity
o Bleeding gums
o Remember: Dracula stories
 Progressive ataxia in childhood
o Ataxic Telangiectasia ---------------------------------------------------------------------- *** TQ

 Autosomal recessive
 Progressive ataxia
 Telangiectasia in the eye and the ear
 Ataxia with cerebellar symptoms
 Bleeding in the eyes because of conjunctiva
 Have infections
The difference between Ataxic Telagiectasia & Von Hippel Landau ------------------------------ *** TQ
Disease Ataxic Telagiectasia Von Hippel Landau

Inheritance Autosomal recessive Autosomal dominant
Ataxia with cerebellar symptoms Ataxia with cerebellar symptoms Ataxia with cerebellar symptoms
Bleeding in the eyes Bleeding in the eyes because of Bleeding in the eyes because of
Telagiectasia of conjunctiva Angiomas in the retina
o Abetalipoproteinemia ---------------------------------------------------------------------- *** TQ

 Progressive ataxia
 Acanthocytes (also present in Chorea acanthocytosis)
 Basophilic stippling in RBCs due to lead poisoning
o Fredrick’s Ataxia --------------------------------------------------------------------------- *** TQ
 Onset before 20
 Autosomal Recessive > Dominant
 Ataxia
 Nydtagmus
 Hammer toe
 Babinski
 Kyphoscoliosis
 Cardiac dysfunction
 In-coordination of hands
 Speech difficulty
 Progressive course  Death after about 15 years
o Neurofibromatosis -------------------------------------------------------------------------- *** TQ

 Neurofibromas on the skin and in the peripheral nervous system, in the nerve roots
& in the CNS
 Bilateral acoustic neruomas & optic nerve neuromas with neurofibromatosis
with lesions in the nervous system and café-au-lait spots
 Shae green patches and leaf-shaped macules (only seen in uv-light)
 No Heart Tumors ***
 Renal artery stenosis
 Thoracic & Abdominal Tumors .
o Tuberous Sclerosis ------------------------------------------------------------------------- *** TQ

 Infantile spasms
 Developmental abnormalities
 Mental Retardation
 Kidney, Heart & Abdomen Tumors
o Sturge - Weber ------------------------------------------------------------------------------ *** TQ

 Port wine stains on the skin
 Arteriovenous inflammation inside the head
Other progressive diseases in children

o Gaucher
 Glucocerebrosides cannot be broken down
• Type I is the most common form (non-neuronopathic)
• Type II: appear several months after birth & usually die by two years old
• Type III: irregular eye movements, seizures & mental retardation.
o Tay Sach’s
 ⇑ increased sensitivity to sound,
 Progressive neurological degeneration with seizures  death
o MCLD
 Inherited CNS demyelination
 Cause of progressive dementia in children.
o Hurler’s Disease
 Mucopolysaccharide problem
o SSPE
 Due to Rubella
 Presents similar to Mad Cow Disease
TORCH
 Neonatal symptoms that occur when mother is infected with these diseases
o Seen in neonates with
 Microcephaly (small head)
 Cerberal palsy
 Chorioretinitis
 Multicysticleukomalacia: Calcifications or holes in the white matter of brain
o T = Toxoplasmosis
 Chorioretinitis
 Diffuse calcifications throughout the brain
 Due to cat excrement exposure
 Occurs in 3rd trimester
o O = Others
 Syphilis
• Occurs in 2nd trimester
• Hutchinson’s Triad
• Deafness
• Teeth decay
• Hydocephalus
• Keratitis
 Varicella
• Cerebellitis
o R = Rubella
 Cataracts
 Chorioretinits
 Coronary heart disease
 Pulmonary abnormalities
 Hepatosplenomegaly
 Jaundice
 Anemia
 Thrombusadopenia
 Rash
 Lethargy
 Hypotonia
 Mental Retardation
 Seizures
 Occurs in 1st trimester
o C = Cytomegalovirus
 Periventricular calcifications: calcifications around the ventricles
 Occurs if 1st trimester
o H = Herpes Simplex
 Chorioretinitis
 Holes in the white matter

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NEUROLOGY

MOTOR OR PYRAMIDAL SYSTEM

 The face, the arm representation is found laterally

 Stroke due to:

  weakness on same side

 III, IV, VI - occulomotor movements

 V CN - Sensation to the face

 VII CN - facial motion

Normal EEG patterns

Ischemic Stroke Subtypes

Lacunar syndromes: (small vessels clots) ---------------------------------------------------------------- *** TQ

Large vessel strokes (Cortical Strokes)

Evaluation of acute stroke patients

Treatment of acute stroke patients

Complications of acute hemorrhagic stroke

Treatment/medications for hemorrhagic stroke

Storkes in children and young adults

Two major groups

Infantile Spasm (West Disease)

Lenox Gastaut - Minor Motor Seizures (Atonic or Myotic seizures)

Absence (Petite Mal) seizures

Grand mal (Tonic Clonic)

Rolandic (ADNFLE) Epilepsy

Other conditions arelated to seizures

Assessment & Evaluation of Head Trauma

Concussion & Contusion

C-Spine Burst Fractures

Acute compression of Spinal Cord

Anterior S/C artery occlusion syndrome ---------------------------------------------------------------- *** TQ

Central cord Syndrome (Syringomyelia) ----------------------------------------------------------------- *** TQ

Management of Coma --------------------------------------------------------------------------------------- *** TQ

Coma With Brain Stem Intact

Coma With Brain Stem NOT Intact

How to tell if brain stem is intact while in coma

Spells - can be differentiated by History:

Focal Neuro signs & Spells occur in

Near syncope/pre-syncope: the sensation is that of "graying-out", lightheadedness, generalized

The distinction between Vertigo & Dizziness

Causes of Peripheral Vertigo

Cataplexy (loss of muscle tone) ------------------------------------------------------------------------------ ***TQ

Metabolic & other disorders that can produce toxicity

SPINAL CORD TUMORS ---------------------------------------------------------------------------------- ***TQ

Most causative organism according to age

 Staph, Strep epidermitis

COMPLICATIONS of Bacterial Meningitis - Neurological Sequele

II. PERIPHERAL NS DEMYELINATION

Peripheral Neuropathy / Neuromuscular Junction

 Duchenne-Becker Dystrophy ---------------------------------------------------------------------- *** TQ

Fascio-Scapulo-Humural (FSH) Dystrophy .

Myotonic Dystrophy ------------------------------------------------------------------------------------------ *** TQ

Myotonia congenita (Thomson’s Disease) ---------------------------------------------------------------- *** TQ

Dermatomyositis ---------------------------------------------------------------------------------------------- *** TQ

Inclusion body Myositis - (all you need to know is the name)

Kearns Sayre Daroff

Mitochondrial encephalopathy with Lactic Acidosis and Strokes (MELAS)

Nerves can be affected by ischemia

Nerve compression in the Upper Extremities

Nerve compression in the Lower Extremities

Hereditary Sensory Motor Neuropathy (Type I, II, III & IV)

Neuro-Muscular junction disorders (Myasthenia Gravis) -------------------------------------------- *** TQ

 Remember in EEG: Three cycle per second is seen in Epilepsy (Petite-Mall)

Floppy baby is born - where is the lesion?

Most important Diseases in Pediatric Neurology