Neurological  
Disorders
Structural Organization
Nervous System Function
Sensory Tracts
Major Sensory Tracts
•	Anterolateral (Spinothalamic)
•	crosses immediately  in the cord
•	sensation is poorly  localized
•	itch, pain, temp
Major Motor Tracts
•	Lateral Corticospinal
•	crosses at medulla
•	innervates distal muscles
•	fine motor control

How Do Neurons Communicate?
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)
Head Trauma / Bleeds
•	Focal: localized
•	Polar: acceleration-deceleration
•	Diffuse:  widespread disruption
Determinants 
of Intracranial Pressure
•	Three space occupying components
•	Brain 
•	CSF 
•	Blood 
•	Compensation for Increased ICP
•	CSF shunt to spinal cord
•	Hyperventilation leading to vasoconstriction
         Causes of Increased ICP
•	Brain infection
•	Rupture of blood vessels
•	Hydrocephalus
•	F & E imbalances

•	Head Injury – most common

                  Types of Injury
•	Primary injury

•	Secondary injury
Pathophysiology 
of Secondary Injury
Compensation for Increased ICP
Progression of S/S of  Increasing ICP
•	Mild to moderate

•	Moderate to severe

•	Severe
    Headache,    LOC, projectile vomiting, localized pain, decorticate posturing

Pupil changes, hyperventilation, decerebrate posturing, seizures

Loss of respiratory control, apnea

Progression of S/S of  Increasing ICP
•	Severe

•	Severe
    Respiratory arrest
Flaccidity
Ischemic response

Brain death
No spontaneous respirations/3 minutes
Fixed pupils
Flat EEG

    Ischemic Response “Cushing’s Reflex”
•	Increased blood pressure

•	Wide pulse pressure

•	Decreased heart rate

•	Loss of respirations
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
General Therapy for Increased ICP
•	Elevate HOB
•	Diuretics
•	Sedation
•	Hyperventilation
•	Decompression

      Classification of Head Injury
•	Concussion
•	Contusion
•	Brainstem Contusion
•	Hemorrhage

  *  Epidural
  *  Subdural

      -  acute
      -  subacute/chronic
Intracranial Bleeds
CVA: Stroke
•	Thrombotic
•	atherosclerosis, assess carotids > age 50
•	Embolic
•	atrial fibrillation, valvular disease, hyper- coagulable states
•	Hemorrhagic
•	structural anomalies
•	hypertension
Stages of Thrombotic Stroke
•	Transient ischemic attacks (TIAs)

•	Stroke in evolution

•	Completed stroke
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
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
Chronic Manifestations of Stroke
•	Contralateral hemiplegia
•	Ptosis
•	Homonymous hemianopsia
•	Neglect
•	Aphasia
•	Loss of bowel and bladder control
•	Emotional Instability
Homonymous Hemianopsia
General Therapy for CVA
•	Get to a Brain Trauma Center
•	Prevention
•	Manage high blood pressure
•	Anticoagulation
•	Rehabilitation
Alzheimer Disease
•	Dementia (deterioration of mentation) 
•	about 70% Alzheimer type
•	others are multi-infarct type (vascular)
•	Manifestations  (JAMICO)
•	judgment		-confusion
•	affect			-orientation
•	Memory
•	Intellect
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
Alzheimer Disease
•	Diagnosis of Exclusion
•	rule out other, potentially treatable causes
•	MRI
•	brain atrophy, enlarged ventricles
•	Poor mental function
•	Mini  Mental State Exam
                       Seizures
•	Partial

  Simple (no   LOC)

  Complex (    LOC)
   Secondarily generalized

•	Generalized

  Absence (Petit Mal) 

  Tonic-Clonic (Grand Mal)
Upper vs Lower Motorneuron
Upper Motor Neuron Disorders
•	Stroke/Head Injury
•	Cerebral Palsy
•	Huntington’s Chorea
•	Parkinson’s Disease
Localization of Motor Dysfunction
•	Reflexes
•	Deep tendon reflexes (cord reflexes)
•	Babinski (corticospinal tract)
•	Strength	
•	focal vs general
•	ipsilateral vs contralateral
•	spasticity vs flaccidity
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
Manifestations of Parkinson Disease
•	Classic Triad (unilateral --> bilateral)
•	Akinesia
•	Rigidity
•	Resting tremor
•	Associated Manifestations
•	Propulsive gait	-  Poor speech quality
•	Masklike face	-  30-50% have dementia
•	Drooling
Features of Parkinson disease
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
Brainstem and Spinal Cord Disorders
•	Multiple Sclerosis

•	Poliomyelitis

•	Spinal Cord Injury
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
Presentation of MS
•	Usually relapsing remitting pattern
•	paresthesias
•	gait disturbance
•	leg weakness
•	vision loss (optic neuritis)
•	double vision 
•	arm weakness
•	vertigo
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
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
Autonomic Dysreflexia
Q:	What Pattern of Sensory-Motor Impairment Would Occur?
Lower Motor Neuron Disorders
•	Bell’s Palsy

Guillian Barre’ Syndrome
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
Disorder of Neuromuscular Junction
•	Myasthenia Gravis
•	80%-90% have anti-receptor antibodies
•	75% have abnormal thymus														
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)
               Muscle Disorders
•	Muscular Dystrophy
Disorders of Hearing
•	Conductive hearing loss
•	otosclerosis
•	otitis media
•	Sensorineural hearing loss
•	Presbycusis
•	Menière Disease
Disorders of Vision
•	Errors of Refraction
•	myopia, hyperopia, presbyopia
•	Cataract
•	Retinal detachment
•	Glaucoma
•	increased intra-ocular pressure
Open Angle Glaucoma
Closed Angle Glaucoma
Open and Closed Angle Glaucoma
             Sensory dermatomes
                 Pain Transmission
•	Gate Theory

Uses the analogy of a gate to describe how impulses from damaged tissues are sensed in the brain.
        Pain Transmission, con’t.
•	Tissue injury stimulates the release of:

 *  Bradykinin
 *  Histamine
 *  Potassium
 *  Prostaglandins
 *  Serotonin
          Pain Transmission, con’t.
•	“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
         Pain Transmission, con’t.

Types of pain are related to the proportion of

                      “A” to “C” fibers

                 in the damaged tissue.
          Pain Transmission, con’t.
         Pain Transmission, con’t.
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!
         Pain Transmission, con’t.

It’s the large, activated “A” fibers that

                   closes the gate

and this will inhibit transmission to the brain and limits perception of 

                          PAIN!
         Pain Transmission, con’t.

It’s the small, activated “C” fibers that

                   opens the gate

and this will allows transmission to the brain and causes perception of 

                          PAIN!
          Pain Transmission, con’t.
•	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.

           Pain Transmission, con’t.
Along with the “A” and “C” fibers, there are
specialized cells that control the GATE – these are the “T” cells, which have a threshold…meaning that impulses must overcome the threshold in order to be sent to the brain.
           Pain Transmission, con’t.
•	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.
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)