Neurological Disorders

1
Neurological Disorders
2
Structural Organization
Cerebral hemispheres
Brainstem Cerebellum
Spinal and Cranial
Spinal Cord
3
Nervous System Function
Brain Central Processing Unit
Sensory Inputs
afferent
efferent
Secretion Movement
4
Sensory Tracts
5
Major Sensory Tracts

• Dorsal column
• ipsilateral until medulla, then crosses
• sensation is well localized
• touch, vibration, pressure,

• Anterolateral (Spinothalamic)
• crosses immediately in the cord
• sensation is poorly localized
• itch, pain, temp

6
Major Motor Tracts

• Medial Tracts
• some tracts cross at medulla, some dont
• innervates axial muscles
• balance, gross motor

• Lateral Corticospinal
• crosses at medulla
• innervates distal muscles
• fine motor control

7
How Do Neurons Communicate?
8
Neurotransmitter Classes

• Acetylcholine
• Amines (DA, NE, E, 5HT, histamine)
• Amino acids (glutamate, GABA, glycine)
• Purines (adenosine)
• Gases (nitric oxide)
• Neuropeptides (Sub P, endorphins, AII, oxytocin,
  many others)

9
Head Trauma / Bleeds

• Focal localized
• Polar acceleration-deceleration
• Diffuse widespread disruption

10
Determinants of Intracranial Pressure

• Three space occupying components
• Brain
• CSF
• Blood
• Compensation for Increased ICP
• CSF shunt to spinal cord
• Hyperventilation leading to vasoconstriction

11
Causes of Increased ICP

• Brain infection
• Rupture of blood vessels
• Hydrocephalus
• F E imbalances
• Head Injury most common

12
Types of Injury

• Primary injury
• Secondary injury

13
Pathophysiology of Secondary Injury

14
Compensation for Increased ICP
Brain Swelling
ICP
CSF shunted to spinal cord
Hyperventilation
CSF in brain ventricles
PaCO2
Cerebral vasoconstriction
ICP
Blood in brain
ICP
15
Progression of S/S of Increasing ICP

• Mild to moderate
• Moderate to severe
• Severe

• Headache, LOC, projectile vomiting,
  localized pain, decorticate posturingPupil
  changes, hyperventilation, decerebrate posturing,
  seizuresLoss of respiratory control, apnea

16
Progression of S/S of Increasing ICP

• Severe
• Severe

• Respiratory arrestFlaccidityIschemic
  responseBrain deathNo spontaneous
  respirations/3 minutesFixed pupilsFlat EEG

17
Ischemic Response Cushings Reflex

• Increased blood pressure
• Wide pulse pressure
• Decreased heart rate
• Loss of respirations

18
Assessment of Brain Function

• Level of Consciousness ABCs
• Manifestations of increased ICP
• headache, vomiting, pupil reactivity
• Glasgow Coma Scale
• Eye Opening
• Best Motor Response
• Verbal Response
• CT scan

19
General Therapy for Increased ICP

• Elevate HOB
• Diuretics
• Sedation
• Hyperventilation
• Decompression

20
Classification of Head Injury

• Concussion
• Contusion
• Brainstem Contusion
• Hemorrhage Epidural Subdural -
  acute - subacute/chronic

21
Intracranial Bleeds
22
CVA Stroke

• Thrombotic
• atherosclerosis, assess carotids gt age 50
• Embolic
• atrial fibrillation, valvular disease, hyper-
  coagulable states
• Hemorrhagic
• structural anomalies
• hypertension

23
Stages of Thrombotic Stroke

• Transient ischemic attacks (TIAs)
• Stroke in evolution
• Completed stroke

24
Manifestations of Stroke

• Acute
• focal neurological signs
• may rapidly change (evolve)
• depends greatly on area of brain damage
• Transient Ischemic Attack (TIA)
• signs and symptoms resolve quickly
• no permanent loss of function

25
Stroke Ischemic vs Hemorrhagic?

• TIA give ASA refer for carotid assessment
• Stroke Get CT scan immediately
• Ischemic evaluate for tPA (within 3 hours)
• embolic and thrombotic
• Hemorrhagic Neurosurgical consult

26
Chronic Manifestations of Stroke

• Contralateral hemiplegia
• Ptosis
• Homonymous hemianopsia
• Neglect
• Aphasia
• Loss of bowel and bladder control
• Emotional Instability

27
Homonymous Hemianopsia
right visual field
left visual field
area of stroke damage
left visual field blindness
28
General Therapy for CVA

• Get to a Brain Trauma Center
• Prevention
• Manage high blood pressure
• Anticoagulation
• Rehabilitation

29
Alzheimer Disease

• Dementia (deterioration of mentation)
• about 70 Alzheimer type
• others are multi-infarct type (vascular)
• Manifestations (JAMICO)
• judgment -confusion
• affect -orientation
• Memory
• Intellect

30
Pathology of Alzheimer Disease

• Genetics VS Environment
• Apo-E gene
• toxins, viruses, aluminum
• Pathological Findings (at autopsy)
• amyloid plaques
• neurofibrillary tangles
• cerebral atrophy and large ventricles

31
Alzheimer Disease

• Diagnosis of Exclusion
• rule out other, potentially treatable causes
• MRI
• brain atrophy, enlarged ventricles
• Poor mental function
• Mini Mental State Exam

32
Seizures

• Partial Simple (no LOC) Complex (
  LOC) Secondarily generalized

• Generalized Absence (Petit Mal)
  Tonic-Clonic (Grand Mal)

33
Upper vs Lower Motorneuron
UMN
LMN
Reflexes Increased Decreased Atrophy No Yes Muscle
tone Spastic Flaccid Fasciculations No Yes
34
Upper Motor Neuron Disorders

• Stroke/Head Injury
• Cerebral Palsy
• Huntingtons Chorea
• Parkinsons Disease

35
Localization of Motor Dysfunction

• Reflexes
• Deep tendon reflexes (cord reflexes)
• Babinski (corticospinal tract)
• Strength
• focal vs general
• ipsilateral vs contralateral
• spasticity vs flaccidity

36
Parkinson Disease

• Etiology
• unknown, possibly neurotoxin
• some suspect pesticide exposure
• MPTP cases of Parkinson-like syndrome
• Pathogenesis
• Low dopamine level in basal ganglia
• Excessive action of acetylcholine
• Disease process is progressive

37
Manifestations of Parkinson Disease

• Classic Triad (unilateral --gt bilateral)
• Akinesia
• Rigidity
• Resting tremor
• Associated Manifestations
• Propulsive gait - Poor speech quality
• Masklike face - 30-50 have dementia
• Drooling

38
Features of Parkinson disease
39
Management of Parkinson Disease

• Drug Therapy is controversial
• Restore Dopamine / Ach balance
• MAOI (selegiline)
• Amantadine (Symmetrel)
• Levodopa, carbidopa (Sinemet)
• anticholinergics (Cogentin, Artane)
• Surgical Techniques
• adrenal medulla tissue transplants

40
Brainstem and Spinal Cord Disorders

• Multiple Sclerosis
• Poliomyelitis
• Spinal Cord Injury

41
Multiple Sclerosis

• Etiology
• Autoimmune attack on CNS myelin
• Pathogenesis
• Immune injury to myelinated neurons
• Sclerotic plaques noted on MRI
• Demyelination disturbs neuron conduction
• Extremely variable course and presentation

42
Presentation of MS

• Usually relapsing remitting pattern
• paresthesias
• gait disturbance
• leg weakness
• vision loss (optic neuritis)
• double vision
• arm weakness
• vertigo

43
Diagnosis and Treatment

• Suspect with episodic neurologic deficits in
  20-40 age group especially Northern European
• MRI lesion is diagnostic
• Treatment symptoms
• Beta interferon may decrease frequency of attacks
• Immune suppression

44
Transection of Spinal Cord

• Spinal Shock (lasts 2-8 weeks)
• loss of spinal cord reflexes below injury
• flaccidity
• decreased vascular tone - hypotension
• atony of bowel and bladder
• Autonomic Dysreflexia
• reflex activation of sympathetic neurons below
  level of injury

45
Autonomic Dysreflexia
stimulus (full bladder)
Reflex vasoconstriction below level of injury
Increased blood pressure
Cant get signal to vessels below injury
x
Baroreceptor Response
bradycardia
vasodilate above SCI
hypertension
46
Q What Pattern of Sensory-Motor Impairment Would
Occur?
47
Lower Motor Neuron Disorders

• Bells PalsyGuillian Barre Syndrome

48
Guillain Barre Syndrome

• Most common cause of acute flaccid paralysis
• Presentation Back leg pain progressing to
  weakness
• decreased DTRs
• Hx viral infection esp. mono preceding
• decreased nerve conduction velocity
• Hospitalize, plasmapheresis, IgG

49
Disorder of Neuromuscular Junction

• Myasthenia Gravis
• 80-90 have anti-receptor antibodies
• 75 have abnormal thymus

Y
Y
Y
50
Myasthenia Gravis

• Presentation NM fatigue which worsens with
  activity eye droop, diplopia, head droop, jaw
  dropping
• No loss of reflexes, no change in sensation
• Respond to edrophonium (fast acting
  anticholinesterase)

51
Muscle Disorders

• Muscular Dystrophy

52
Disorders of Hearing

• Conductive hearing loss
• otosclerosis
• otitis media
• Sensorineural hearing loss
• Presbycusis
• Menière Disease

53
Disorders of Vision

• Errors of Refraction
• myopia, hyperopia, presbyopia
• Cataract
• Retinal detachment
• Glaucoma
• increased intra-ocular pressure

54
Open Angle Glaucoma
fluid
Increased anterior chamber IOP
clogged canal of Schlemm
55
Closed Angle Glaucoma
fluid
Increased anterior chamber IOP
plugged canal of Schlemm when pupil dilates
(acute)
56
Open and Closed Angle Glaucoma
57
Sensory dermatomes
58
Pain Transmission

• Gate Theory Uses the analogy of a gate to
  describe how impulses from damaged tissues are
  sensed in the brain.

59
Pain Transmission, cont.

• Tissue injury stimulates the release of
  Bradykinin Histamine Potassium
  Prostaglandins Serotonin

60
Pain Transmission, cont.

• A Fibers myelin sheath large fiber
  size conduction is fast inhibits pain
  transmission Sharp well- localized

• C Fibers no myelin sheath small fiber
  size conduction is slow facilitates pain
  transmission dull non-localized

61
Pain Transmission, cont.

• Types of pain are related to the proportion
  of A to C fibers
  in the damaged tissue.

62
Pain Transmission, cont.
These two pain fibers enter the spinal cord at
the dorsal horn and travel up to the brain.This
is the location of the GATE
63
Pain Transmission, cont.

• The gates regulate the flow of sensory impulses
  to the brain! If the gate is closed no
  impulses get through. Therefore no impulses
  are transmitted to the higher centers in
  the brain so there is no perception of PAIN!

64
Pain Transmission, cont.

• Its the large, activated A fibers that
  closes the gateand this will
  inhibit transmission to the brain and limits
  perception of PAIN!

65
Pain Transmission, cont.

• Its the small, activated C fibers that
  opens the gateand this will
  allows transmission to the brain and causes
  perception of PAIN!

66
Pain Transmission, cont.

• Nerve fibers from the brain innervate the GATE
  and allow the brain some control over the
  GATE.in that the brain can evaluate the
  pain identify the type of pain localize
  the pain
• This also allows the brain to control the GATE
  before the gate is open.

67
Pain Transmission, cont.

• Along with the A and C fibers, there
  arespecialized cells that control the GATE
  these are the T cells, which have a
  thresholdmeaning that impulses must overcome the
  threshold in order to be sent to the brain.

68
Pain Transmission, cont.

• Body produces endogenous neurotransmitters
  Enkephalins Endorphins
• They are produced by the body to (1) fight
  pain (2) bind to opioid receptors (3) inhibit
  transmission of pain impulses by closing
  the GATE.

69
Measures to ? Close the GATE

• Rubbing the painful area(this inhibits the large
  A sensory fibers
• Give the opiates to close the GATE(this will
  reduce recognition of pain)

70
Hang in there just one more week!!