BRAIN DAMAGE

1

BRAIN DAMAGE
2

• Traumatic brain Injury (TBI)
• Stroke/Aneuryism
• Anoxia
• Cancer
• Disease
• Development

3
TBI
Common sources of Traumatic Brain Injuries

• Traumatic Brain Injury (TBI) is a leading cause
  of death and disability
• among children and young adults in the United
  States.
• Each year, an estimated 1.5 million Americans
  sustain a TBI.
• That's 8 times the number of people diagnosed
  with breast cancer
• and 34 times the number of new cases of HIV/AIDS
  each year. 
• As a consequence
• 50,000 people die each year.
• 230,000 people are hospitalized annually and
  survive.
• 80,000 to 90,000 people experience the onset of
  long-term
• disability each year.
• The cumulative result is that today an estimated
• 5.3 million people - 2 of the U.S. population -
  are living with a permanent TBI-related
  disability.
• The risk is highest among adolescents, young
  adults, and persons older than 75 years. The risk
  to males is twice the risk among females.

4
Typical to TBI the trauma may involve damage
associated with the initial blowCoup
5
And rebound damage caused to the opposite side of
the braincontra coup
6
TBI- physical effects
Bruising Swelling Shearing Misalignment Anoxia nec
rosis
7
TBI is associated with contusions and hematoma
That may cause brain swelling and cell death.
8
Reducing intracranial pressure may reduce damage
9

• TBI also may cause tearing (shearing) of axon
  tracts

10
GCS-gauging the severity of damage
11
Unfortunately many victims of head trauma do not
exhit immediate obvious symptoms -Post concussive
syndromes
12
Case studies of PCS- Auto accident

• Melissa spent the next day spraying vomit into
  her bedpan and vehemently denying anything was
  wrong with her. She laughs and cries and rages
  within moments of one another and complains that
  she cannot see the ceiling
• Cat scans failed to find conclusive indication of
  brain damage.diagnosed as PCS.
• ....the accident shook, turned and rattled her
  brain, causing widespread disruptions on
  microscopic levels. Detailed scans a year later
  will reveal that Melissas brain was riddled with
  focal defects, pockets of arbitrarily traumatized
  tissue encapsulated within healthy brain.
  Sheering injuries in her occipital lobe disrupted
  key functioning in her visual cortex diffuse
  axonal injuries severed untold neural connections
  within the right frontal lobe, compromising her
  self-regulation. Cellular injuries to her
  parietal lobe interrupted the normal processing
  of sensory input
• prior to the accident , Melissa was a paragon of
  modern womanhood, the emodiment of every
  contemporary virtue.
• I was a real catch she says, gigling a little..
  A master swimmer, cross-country skier, white
  water kayaker..had won awards in writing, public
  speaking. Ambition filled her veins,
  self-reliance and independence exuded from her
  smile.
• Over the course of the next days/weeks..Melissa
  developed a stutter, moved about as if under
  sedation, had lost coordination to the point that
  picking up a coffee mug was a challenge, had
  problems of equilibrium
• ..returned to work 2 months laterfumbled with
  her office keys (they all looked the same to her)
  , could not read (understand) a memo, became lost
  in the hallways, forgot the names of coworkers..
• ..cried a small provocations, snapped at her
  assistant

13
STROKE /CEREBROVASCULAR ACCIDENT
Transient ischemic attack (TIA) refers to
temporary brain dysfunction lasting no longer
than 24 hours due to a shortage of blood and
oxygen. It sometimes is referred to as a
"mini-stroke." TIA is a serious condition that
serves as a warning for a stroke. About 30 of
stroke patients have had a TIA at some point in
the past. Stroke/cerebrovascular accident
(CVA) is a brain injury that occurs when the
brain's blood supply is interrupted. Without
oxygen and nutrients from blood, brain tissue
starts to die rapidly (usually in less than 10
minutes), resulting in a sudden loss of
function.
14
(No Transcript)
15
(No Transcript)
16
Two Major Types of Stroke
17
Results of brain hemorrhage
18
Risk Factorsfor Stroke

• High blood pressure (the number one risk factor
  for ischemic stroke)
• Drug abuse (heroin, cocaine , amphetamines)
• Narrowing of arteries supplying the brain due to
  atherosclerosis
• High cholesterol levels , particularly
  low-density lipoprotein (LDL) cholesterol
• Smoking
• Diabetes mellitus
• Atrial fibrillation (abnormality of heart rhythm)
  
• Use of birth control pills if you are over 35
  years old and smoke
• Long-term use of hormone replacement therapy²

19
Symptomsof Stroke-

• Visual disturbances like blindness in one eye,
  and/or blurry, dimming or double vision.
• Weakness, numbness, or tingling of the face, arm,
  leg, or one side of the body (usually affects one
  side of the body, but there are exceptions).
• Difficulty speaking or understanding words
• Difficulty swallowing
• Dizziness, unsteadiness of gait, loss of balance
  or falling
• Trouble with balance or coordination
• Loss of consciousness
• Nausea and/or vomiting
• Sudden confusion or loss of memory
• Seizures
• Severe or unusual headache

20

• Brain stem stroke damage resulting from partial
  occlusion of the pontine arteries and basilar
  artery and complete occlusion of one pontine
  artery. Tissue damage due to lack of blood supply
  of the pontine area of the brain stem is a cause
  of locked-in syndrome (basilar artery syndrome).

21
Persistent vegetative State (PVS) syndromes vs.
Locked in Syndrome
Locked-in syndrome (Severe brainstem injuries)
individual is alert but can not control movement
or functionexcept sometimes eyeblinks (the
waking nightmare). PVS severe cortical damage
leaves patient without consciousness, but
subcortical processess are intact so that eating,
drinking, even laughing/crying may occur as
reflexive/automatic behaviors (waking death).
22
RX for Stroke?

• MedicationsClot-dissolving drugsgiven within
  three hours of the onset of symptoms. (Note Only
  in carefully selected patients.) Tissue
  plasminogen activator (tPA) is given through a
  vein after the doctor has confirmed the stroke's
  cause and there is no evidence of bleeding.
• Blood-thinning drugs (Anticoagulants)Clexane is
  given by subcutaneously (along with tPA, if
  indicated) and an oral medication (warfarin) is
  sometimes started if long-term treatment with a
  blood-thinner is anticipated.
• Antiplatelet drug aspirin is the most common,
  but clopidogrel (Plavix), dipyridamole
  (Persantine) are also sometimes used.
• Blood pressure medication(usually use Labetalol,
  the first-line drug, or sodium nitroprusside)
• Diabetes mellitus medication
• Drugs that reduce brain swelling
• Medication to control or correct irregular heart
  rhythm (such as atrial fibrillation)
• Cholesterol-lowering medications
• Other interventions during an acute stroke
  include Providing adequate oxygenTaking
  precautions to prevent chokingFrequent
  neurological examinations

23
Deep brain stimulation for comatose victims of
brain damage?

24
Brain Neoplasms

• Types of Primary Brain Tumors
• Primary brain tumors arise from the tissues of
  the CNS - rather than originating from cancerous
  cells that travel from elsewhere in the body.
• Primary brain tumors are categorized as either
  benign (noncancerous) or malignant (cancerous). 
• noncancerous primary brain tumors still can have
  devastating physical and emotional effects. 
• For most patients, there generally is no obvious
  exposure or risk factor that can be linked to
  these tumors.

25
CAT Scan showing a Right Hemispheric Brain Tumor
26
(No Transcript)
27

• Until recently, many brain tumors were considered
  inoperable. The tumors were either so deep that
  conventional surgery to completely remove them
  would damage critical parts of the brain, or the
  tumors were so densely entangled with blood
  vessels that surgery would likely cause a fatal
  brain hemorrhage. Fortunately, scientists have
  discovered a high-tech, non-invasive tool that
  makes such risky surgeries far less dangerous.
  Photon surgery is a form of stereotactic
  radiosurgery -- that is, a non-invasive treatment
  of precisely focused X-rays used to treat brain
  tumors.

28
Minimally invasive brain surgery?
29
Bacterial and Viral Infections of the Brain

• Following are descriptions of some bacterial and
  viral infections.
• I do not require that you memorize specific
  bacterial or viral infections.
• You should recognize that this is a meaningful
  source of damage to the CNS.

30
Bacterial Meningitis

• Certain bacteria can cause an infection in the
  meninges.
• a serious infection that can cause death within
  hours.
• Causes
• The bacteria first cause an upper respiratory
  tract infection . Then it travels through the
  blood stream to the brain.
• You do not need to memorize these, but you may be
  interested
• Streptococcus pneumoniae (the bacteria that
  causes pneumonia )
• Neisseria meningitidis
• Haemophilus influenzae b (Hib)
• In the US, widespread immunization has almost
  eliminated meningitis due to Hib
• Listeria monocytogenes meningitis
• Escherichia coli meningitis ,
• Mycobacterium tuberculosis meningitis
• In general, meningitis is not spread by casual
  contact.

31
Symptomscan develop over several hours, or 1 to
2 days High fever Headache Very stiff, sore
neckOther symptoms may include Red or purple
skin rash Cyanosis (bluish skin color) Nausea
Vomiting Photophobia (sensitivity to bright
lights) Sleepiness Mental confusion
32
Viral infection

33
Rabies virus

• Rabies is an infectious disease of animals. Man
  is occasionally infected, and once infection is
  established in the CNS, the outcome is almost
  invariably fatal.
• HUMAN RABIESIs acquired from virus in saliva
  entering a bite wound caused by an infected
  animal, usually a rabid dog. The severity of the
  bite determines the risk of infection. The
  disease does not usually spread from man to man.
• IncubationAfter inoculation, the virus enters
  small nerve endings at the site of the bite. The
  virus slowly travels up the nerve to reach the
  CNS where it replicates and then travels down
  nerves to the salivary glands where there is
  further replication. The incubation period may
  last from two weeks to six months. Very often the
  primary wound is healed and forgotten by the time
  of clinical presentation.
• Clinical PresentationA) Furious Rabiesheadache,
  fever, irritability, restlessness and anxiety.
  This may progress to muscle pains, salivation and
  vomiting. After a few days to a week the patient
  may experience a stage of excitement and be
  wracked with painful muscle spasms, triggered
  sometimes by swallowing of saliva or water. The
  stage of excitement lasts only a few days before
  the patient lapses into coma and death. Once
  clinical disease manifests, there is a rapid,
  relentless progression to invariable death,
  despite all treatment.
• B) Dumb RabiesStarts in the same way, but
  instead of progressing into excitement, the
  subject retreats steadily and quietly downhill,
  with some paralysis, to death. Rabies diagnosis
  may easily be missed.

34

• Viral meningitis
• A relatively mild disease with a good prognosis.
  Patients present with fever, headache, neck
  stiffness and photophobia. Common viral agents
  include enteroviruses, mumps virus and
  lymphocytic choriomeningitis virus.
• Acute necrotizing encephalitis Infection of the
  brain by HSV. Neurons of the temporal lobe are
  most commonly involved. Infection is severe and
  necrotising. Clinical features include sudden
  onset of fever, headache, confusion and
  alteration in personality. Mortality is high and
  neurological impairment in the survivors is
  invariable. Encephalitis may be due to primary
  infection or reactivation.

35
Progressive multifocal leuco-encephalopathy
The Papovavirus family contains two main
groups-Papilloma viruses (which cause
warts)Polyoma viruses, these are slightly
smaller than papilloma viruses, and in animals
are sometimes associated with tumours. The two
known human polyoma viruses are JC - Progressive
multifocal leuco-encephalopathy BK - isolated
from urine of immunosuppressed patients dsDNA
genome small icosahedral particles, 42-45 nm
grows in human foetal glial cell cultures (JC)
Progressive multifocal leuco-encephalopathy is a
progressive neurological disorder caused by
reactivation of JC virus in the brain. Infection
is common, but neurological disease is rare it
only occurs in immunosuppressed patients.
Clinical FeaturesPatients may present with a
variety of neurological signs, including
hemiparesis, dementia, dysphagia, muscular
inco-ordination or impaired vision. The condition
is progressive and invariably fatal.
PathologyMultiple foci of demyelination are
found throughout the cerebral hemispheres and
cerebellum. The virus infects oligodendrocytes,
which have a bizzare histological appearance.
EpidemiologyInfection with JC virus is common,
but invariably asymptomatic Seroprevalence
surveys have shown that about 50-60 of adults
have antibodies.
36
Retrovirus Disease Lentivirinae Lentiviruse
s characteristically establish a persistent
infection in the host and cause chronic wasting
disorders which are uniformly fatal.
PathologyInflammatory cell infiltration,
perivascular cuffing of blood vessels,
demyelination, necrosis and reactive gliosis.

Virus Host Clinical Features
Visna-Maedi virus sheep paralysis, wasting, ataxia
Caprine arthritis encephalitis virus (CAEV) goats paralysis, wasting, ataxia
HIV 1 and 2 humans dementia
37
Kuru This is a transmissable prion disease found
only in the Fore people of New Guinea. It first
appeared about 60 years ago and the incidence
increased until the late 1950's. The disease is
now known to have been transmitted through ritual
cannibalism until the late 1950's it was the
practice of women and children to eat the brains
and viscera of dead relatives, including those
who had themselves died of Kuru. Cannibalism
stopped in 1957 and the incidence of Kuru has
declined sharply since then. Clinical
featuresThe incubation period varied from 4-20
years. Patients presented with progressive
cerebellar dysfunction. Death usually occurred
within a year of initial presentation.
Transmission studiesIntra-cerebral inoculation
of brain tissue from Kuru victims into non human
primates leads to the development of symptoms
within two years.
38
Creutzfeldt-Jakob disease (CJD) In 1920,
Creutzfeldt described a progressive dementing
illness in a 22 year old woman. The following
year, Jakob described four older patients with a
clinically similar presentation and course. Since
then, numerous cases of CJD have been described.
CJD occurs world wide. It is very rare, with an
incidence of about 1 case per million population.
While most cases are sporadic, 5-10 are
familial. In the familial form, CJD is inherited
as an autosomal dominant condition. Clinical
featuresThe onset of the disease typically
occurs between the ages of 50 and 65 years. There
are two main modes of presentation 1. Chronic
dementing illness 2. Progressive cerebellar
dysfunction The condition is relentlessly
progressive and patients usually die within a
year of presentation. Transmission The natural
route of infection is not known, but CJD has been
accidently transmitted by1. Corneal grafts -
where the corneas were harvested from cadavers
that died of CJD.2. Growth hormone preparations,
derived from human pituitary glands.3. In two
patients who received grafts of dura mater,
prepared from cadavers, and4. through electrodes
used for electro-encephalography which had
previously been used in a patient with CJD. The
prion detected in the brains of patients with CJD
is termed PrPCJD. The disease has also been
experimentally transmitted to chimpanzees and
other primates. Following intracerebral
inoculation, the incubation period is 11-14
months. The disease can also be transmitted
peripherally (IV, intra peritoneal or
intramuscular routes). But transmission is much
less efficient and the incubation period is much
longer (many years).
39
General Functional Effects of Brain damage-
largely depend on what brain region is involved-
You should be able to characterize the following
deficits

• Anomias
• Functional deafness
• Aprosodias
• Asomatognosia
• Unilateral neglect
• VIsual hemi-neglect
• Apraxias
• hemiplegia
• Amnesias
• Changes in Affect
• Loss of Judgement
• Impulsivity
• Bizarre behaviors
• Aphasias
• Anosagnosias
• Etc...

40

• Brainstem syndromes
• Wallenbergs (lateral medullary) CN5
  (ipsilateral facial analgesia), 8 (vertigo), 9,
  10 (hoarse,etc), sympathetics (ipsilateral
  Horners), solitary nuc. (taste), cuneate/gracile
  nuc. (ipsilateral numbness), spinothalamic tract
  (contralateral pain/ temp loss only 1
  contralateral) no weakness
• Webers ventral midbrain CN3 w/crossed
  hemiplegia
• Claude dorsal midbrain CN3 w/ataxia
• Benedikts CN3 w/ ataxia and hemiplegia
• Parinauds upgaze palsy, loss of accomodation
  (fixed pupils) only 1, large pupils w/ light/
  near dissociation, convergence nystagmus,
  nystagmus retractorius, lid retraction
• Millard-Gubler base of pons, CN6 7 and
  contralateral hemiplegia
• Medial medullary contralat hemiparesis (not
  face), contralat numbness, ipsi CN12
• Lateral pontine (SCA) ipsi ataxia, contralat
  pain/temp, deafness, N/V
• Locked-in Bilateral basilar pons
• Pseudobulbar palsy lesion of bilateral UMN
  corticobulbar tracts above brainstem (eg IC)
  unable to move eyes, mouth but can yawn cry
  (reflexive). Brisk jaw-jerk/reflexes. Also
  frontal signs, emotional lability may occur due
  to adjacent frontal fiber damage.
• Bulbar palsy LMN CN palsy (usu IX-XII)
• Top-of-the-Basilar sudden onset AMS, EOM/ pupil/
  visual (homonymous hemianopsia) abnormalities,
  usu. Embolic.
•  
•  
• Brainstem Reflexes
• Pupil 2 3.
• Dolls 3 8 (VestNuc gt PPRF gt CN3/6).
• Jaw-jerk 5 only.