neurological disorder

1. NEUROLOGICAL
DISORDERS
PATHOPHYSIOLOGY
Presented by
Sarafeen Akram
Arooj Patras
Urfa Khursheed Robert

2. .
TOPIC :
PAIN
.Somato-sensory Pathway
.Functions of Noci-ceptors in response to
pain information

3. Definition:
PAIN is an unpleasant sensory and
emotional experience associated
with actual and potential tissue
damage .
Types :
- Acute Pain
- Chronic Pain

4. Causes :
Acute pain often results from injury
, surgery or invasive medical
procedures or can be due to any
infection ,
(pharyngitis ).
Chronic pain can be symptomatic
of a wide range of health problem (
arthritis , back injury ).

5. Pain Receptor : ( NOCICEPTORS )
Theses are group of sensory neurons with
specialized nerve endings widely distributed in
the skin , deep tissues (muscles , joints) and
visceral organs .
Types :
In the CNS there are 3 types of pain
receptors which regulate the
neurotransmission of pain signals .
1. mu
2. kappa
3.delta

6. .
Location of pain receptors :
Similar to mu opioid receptors kappa
and delta opioid receptors reside in the
periphery of dorsal root ganglion , the
spinal cord and in supra-spinal region
associated with pain modulation.

7. Functions of pain receptors:
A noci-ceptor is a sensory neuron
that responds to damaging or
potentially damaging stimuli by
sending possible threats signals
to the spinal cord and the brain .

11. Antero-lateral Pathway
Definition :
The anterolateral pathways (anterior and
lateral supino-thalamic pathway) consist
of bilateral , multi-synaptic , slow-
conducting tracts . These pathways
provide transmission of sensory
information such as pain , thermal
sensations , crude touch , and pressure
that does not require discrete localization
of signals source or fine discrimination of
intensity .

12. . It refers to a collection of ascending pathways that
carry pain and temperature as well as related touch-
sensations from the spinal cord to brainstem or
thalamus .
It is generally considered to contain the :
1. Spino-thalamic tract
2. Spino-reticular tract
3. Spino-mesencephalic tract

13. 1 . Spinothalamic tract
It is an ascending pathway of the spinal
cord.
Together with the medial lemnicus ,it is
one of the important sensory pathways
of the nervous system . It is responsible for
the transmission of pain , temperature and
crude touch to the somatosensory region
of the thalamus .

14. 2 . Spinoreticular tract
It is an ascending pathway in the white
matter of the spinal cord , positioned
closely to the lateral spinothalamic tract.
This tract is form spinal cord –to
reticular formation – to thalamus .
It is responsible for automatic reponses to
pain , such as in case of injury .

15. 3. Spinomesencephalic tract
It is a part of anterolateral pathway . It
terminates in the periaqeductal gray of the
midbrain. The periaqeductal gray is
thought to be an area that is important to
inhibit or controlling pain sensation.

16. Originates :
The fibers of the anterolateral pathway
originates in the dorsal horns at the level
of the segmental nerve , where the dorsal
root neurons enter the spinal cord.
They cross in the anterior commissure ,
within a few segments of origin , to the
opposite anterolateral pathway , where
they ascend upward toward the brain.

17. Also :
These tracts also stimulate autonomic
nervous system responses such as ;
. rise in heart rate
.rise in blood pressure
. dilation of pupils
.the pale and moist skin ( results from
constriction of the cutaneous blood
vessels )
. activation of the sweat glands

18. Subdivisions :
There are two subdivisions in the
anterolateral pathway .
1. Neospinothalamic Tract
2. Paleospinothalamic Tract

19. 1. Neo-spinothalamic Tract
The neo-spinothalamic tract consists of a
sequence of at least three neurons with
long axons. It provides for relatively
rapid transmission of sensory information
to the thalamus.
. It conducts fast pain ( via delta fibers )
and
provide information of the exact location
of
the noxious stimulus .
Noxious …….. Harmful , Unpleasent

20. 2 . Paleospinothalamic Tract
The paleospinothalamic tract ,which is
phylogenetically older than the
neospinothalamic system , consists of
bilateral , multi-synaptic , slow –
conducting tracts that transmit sensory
signals that do not require discrete
localization or discrimination of fine
gradations in intensity.
. It is a multisynaptic tract that conduct
slow pain ( via C fibers ) a pain which is
poorly localize in nature .

21. Central Processing of
Somatosensory Information
Perception , or the final processing of
somatosensory information involves awareness
of the stimuli , localization and discrimination of
their characteristics ,and interpretation of their
meaning .
.The full localization ,discrimination of the
intensity and interpretation of the meaning of
the stimuli require processing by the
somatosensory cortex .

22. .
location :
The somatosensory cortex is located in
the parietal lobe ,which lies behind the
central sulcus and above the lateral
sulcus .
Primary somatosensory cortex
:
The strip of parietal cortex that borders
the central sulcus is called primary
somatosensory cortex because it
receive primary sensory information by
direct projection from the thalamus .

23. . Parallel to and just behind the
primary somatosensory cortex ( i.e
towards the occipital cortex ) lie the
somatosensory association
areas , which are required to
transform the raw material of
sensation into meaningful learned
perception .

24. Sensory Modalities
Definition :
When information from different primary afferents
reaches the forebrain , where subjective experience
occurs , the qualitative differences between warmth
and touch are called sensory modalities .
Somatosensory experience can be divided
modalities , a term used for qualitative ,
subjective distinctions between sensations such
as touch , heat , and pain . These experiences
require function of sensory receptors and
forebrain structures in the thalamus and
cerebral cortex .

25. .
Also :
Sensory experience also involves quantitative
sensory discrimination or the ability to
distinguish between different levels of sensory
stimulation .
- They can initiate action potentials to many
forms of energy at high energy levels , but they
usually are highly tuned to be differentially
sensitive to low levels of a particular energy type
.

26. Stimulus Discrimination
It involes the ability to distinguish between
one stimulus and similar stimulus
……In both cases , it means responding only
to certain stimuli, and not responding to
those that are similar.
.The ability to discriminate the location of a
somethetic stimulus is called acuity and is
based on the sensory field in a dermatome
innervated by an afferent neuron .

27. . High acuity ( i.e the ability to make fine
discrimination of location )
Requires
A high density of innervation by afferent
neurons
. High acuity also requires a projection system
through the CNS to the forebrain that preserves
distinctions between levels of activity in
neighboring sensory fields.

28. Tactile Sensation
Definition :
It refers to the sense of touch , specifically the
information received from varying pressure or
vibration against the skin .
.Tactile sensation is considered a somatic
sensation , meaning it originates at the surface of
the body , rather then internally .

29. The tactile system, which relays sensory
information regarding touch ,pressure , and
vibration ,is considered the basic somatosensory
system .
There are at least six types of specialized tactile
receptors in the skin and deeper structures –
free nerve endings .
1. Meissner corpuscles
2. Merkel disks
3. Pacinian corpuscles
4. Hair follicle end organs
5. Ruffini end organs
6. Free nerve endings

30. Thermal Sensation
Thermal sensation is discriminated by three
types of receptors – cold , warmth , and pain.
. The cold and warmth receptors are located
immediately under the skin at discrete but
separate points . In some areas , there are
more cold receptors than warmth receptors .

31. .
Thermal afferents , with receptive thermal
endings in the skin , send their central axons into
the segmental dorsal horn of the spinal cord. On
entering the dorsal horn , thermal signals are
procrssed by second – order input association
neurons. These association neurons activate
projection neurons whose axons then cross to
the opposite side of the cord and ascend in the
multisynaptic , slow –conducting anterolateral
system to the opposite side of the brain.

32. Position Sensation
Definition :
Position sense refers to the sence of limb and
body movement and position without using
vision. It is mediated by input from
propriceptive receptors ( muscle , spindle
receptors and golgi tendon organs ) found
primarily in muscles , tendons ,and joint
capsules.

33. There are two submodalities of proprioception-
1. Stationary or static component
( limb position sense )
2. Dynamic aspects of position sense
( kinesthesia )
. Both of these depend on constant transmission
of information to the CNS regarding the degree
of angulation .

34. .
.Signals from these receptors are processed
through the dorsal column-medial lemniscus
pathway. They transmit signals from the
periphery to the cerebral cortex ,which are then
processed in the thalamus before reaching the
cerebral cortex .
.Lesions affecting the posterior column impair
position sense . The vestibular system also plays
an essential role in position sense .

35. Functions of Nociceptors
Definition :
These are the sensory receptors that are
activated by noxious stimuli that damage or
threaten the body’s integrity…..
They are classified according to their
responses to mechanical , thermal and chemical
stimuli .

36. .
. There are two types are nociceptive pain :
1 . Somatic pain
Pain from skin , muscles , tendons
and superficial area of the body .
2 . Visceral pain
Pain which originates from your
internal organs .

37. .
Types :
Mechanical
* Strong pressure , sharp objects
Thermal
* Burning heat (>45 C)
* Noxious cold (variable)
Chemical
* pH extremes
*Environment irritants
* Internal neuroactive substances

38. .
Functions :
Specialized peripheral sensory neurons known
as nociceptors ……. that alert us to
potentially damaging stimuli at the skin by
detecting extremes in temperature and pressure
and injury related chemicals , and transducing
thses stimuli into long –ranging electrical signals
that are relayed to higher brain centers .

39. CEREBRAL CIRCULATION

40. CEREBRAL CIRCULATION
Arterial supply
Cerebral arterial supply is done by three arteries.
1. Anterior Cerebral Artery
It supply the medial surface of frontal and
parietal lobes , anterior half of thalamus , corpus
striatum , corpus callosum , anterior limb of
internal capsule.
2. Middle Cerebral Artery
It supply the lateral basal ganglia , insula

41. CONTINUE……………….
and inferior frontal gyrus.
3. Posterior Cerebral Artery
It supply the remaining occipital lobe , inferior
regions of temporal lobes and thalamus.
VENOUS DRAINAGE
Venous drainage is done by following veins
1. Deep Cerebral Venous System
2. Superficial Venous System

42. BLOOD BRAIN BARRIER

43. BLOOD BRAIN BARRIER
DEF It is highly selective semipermeable border
of endothelial cells that prevents solutes in
circulating blood from non-selectively crossing
into the extracellular fluid of the CNS.
 BBB depends on brain capillaries.
 Endothelial cells of brain capillaries are joined
by continuous tight junctions.
 Brain capillaries are surrounded by a basement
membrane and process of supporting cells of
brain called astrocytes.

44. .
CONTINUE…………………..
 Cerebral capillaries are much more permeable
at birth than adult. BBB develops during early
year of life.
 Water soluble compounds excluded from brain
such as cate-cholamines.
 Lipid soluble molecules cross lipid layer of BBB
such as antibiotic chloramphenicol.
 Other medication have a low solubility in lipids
and enter brain slowly.
 Alcohol , nicotine and heroin are very lipid
soluble and enter brain easily.

45. STROKE

46. STROKE
 Stroke is also known as brain attack.
 By WHO stroke is defined as
It is a neurologic deficit due to local
disturbance in blood supply to the brain. Its onset
is usually abrupt but may extend over a few hours
or longer.
 Stroke is of two types.
1. Ischemic Stroke
2. Hemorrhagic Stroke

47. ISCHEMIC STROKE
Where the blood supply to a part of brain suddenly
becomes inadequate for the brain to function
normally.
It results from / causes
 Thrombosis
 Cerebral Embolism
 Ischemia

48. HEMORRHAGIC STROKE
Where a blood vessel ruptures and blood rushes
either through the brain tissue destroying it or
outside the brain itself into the subarachnoid
space.
CAUSES
 Hypertension
 Weak vessel walls
 Age more than 55
 Arteriovenous Malformations

49. RISK FACTORS OF STROKE
 High serum cholestrol level
 Diabetes Mellitus
 Cigarette smoking
 obesity
 Cardiac Diseases
 Sex [ common in males ]
 Race
 Prior Stroke
 Family History
 Hyper-coagulopathy
Hypertension

50. CLINICAL
MANIFESTATION
 Sudden severe headache
 Difficulty in speaking
 Visual field deficits
 Impairment of sensation
 Impairment of mental activity
 Impairment of memory and behavior
 Depression
 Motor loss [ disturbance of voluntary control
and paralysis ]

51. .
CONTINUE………………
 Cognitive Impairment and Psychological
effects are seen in the patient.
DIAGNOSTIC EVALUATION
 History and neurologic examination
 CT Scan , MRI
 cerebral angiography
 Lumbar puncture
 Routine investigation of urine analysis , CBC ,
cholestrol and triglyceride level in blood.

53. TRANSIENT ISCHEMIC
ATTACK
Transient episodes of neurologic dysfunction
caused by focal brain , spinal cord or retinal
ischemia without acute infarction.
 Causes are same as of Ischemic stroke.
 It is an alarm for impending stroke.
 After TIA , there are 50 percent chances to
have stroke within 48 hrs or 10 to 15 percent
with in 3 months.

54. ..
CONTINUE………………
 Surgical treatment is required before the stroke
occurs.
 Medical Interventions should be applied to
prevent eventual stroke or neurologic deficits.

55. TRAUMATIC BRAIN
INJURY

56. TRAUMATIC BRAIN
INJURY
It is a disruption in the normal function of the
brain that can be caused by a blow , bump to the
head suddenly and violently hitting an object or
when an object pierces the skull and enters brain
tissue.
CAUSES
 Falls
 Motor Vehicle Crushes
 Sports Injuries
 Being Struck
 Blast Injuries

57. .
SIGN AND SYMPTOMS
oHeadache
oDizziness
oBlurry vision
oNausea , vomiting
oRinging in ears
PATHOPHYSIOLOGY
 Direct tissue damage- impaired regulation of
cerebral blood flow and metabolism
 Ischemia-like pattern

58. .
 Accumulation of lactic acid
 Increased membrane permeability
 Odema formation
LAB TESTING
oPlasma test
oEvaluation of thinking
oMotor function
oSensory function
oCo-ordination
oReflexes
oCT Scan , MRI scan

59. NURSING MANAGEMENT
Monitor and maintain vital signs and
fluid balance
GCS- level of consciousness
Maintain the sterility of dressings and
drain
Prevent from infection
Medications as ordered
Elevate the head of bed-side
Monitor and maintain ICP

60. MEDICAL MANAGEMENT
ANTIHYPERTENSIVES
 Reduce blood pressure to prevent exacerbation
Of intra-cerebral hemorrhage in hypertensive
encephalopathy
DIURETICS
 Mannitol
ANTICONVULSANTS
 Reduce the frequency of seizures and
prophylaxis of seizure

61. .
CONTINUE…………………
ANTIPYRETICS
 To relief pain and fever
ANTACIDS
 Prophylaxis for gastric ulcer
GLUCOCORTICOIDS
 May help to reduce head and neck ache

62. TYPES
Following are the types.
1. Epi-dural Hematoma
2. Sub-dural Hematoma
3. Parenchymal Trauma
i- Consussion
ii- Laceration
iii- Traumatic Intracranial Hemorrhage
iv- Diffuse Axonal Injuiry

63. EPIDURAL HEMATOMA
It is the localized collection of blood between
skull and dura matter. It is usually the result
of rupture of middle meningeal artery.
It cause rapid rise in intracranial pressure.
If not immediately drained , it will produce
brain herniation.

64. SUBDURAL
HEMATOMA
It is the collection of blood between the
dura matter and arachnoid matter ,
resulting from blunt trauma without
skull fracture causing rupture of some of
the bridging veins that connect the
venous system of the brain with the large
venous sinuses that are enclosed with in
the dura.

65. PARENCHYMAL
TRAUMA
Trauma to brain itself can be grouped under
following headings.
CONCUSSION
Transient loss of consciousness that occurs
immediately following head trauma by blunt
force.
 LACERATION
It is a tear produced by a penetrating object. It
is

66. .
CONTINUE………………..
the injury to CNS tissue with subsequent
hemorrhage and necrosis.
TRAUMATIC
INTRAPARENCHYMAL
HEMORRHAGE
They are contained with in the brain and don’t
extend to the surface probably resulting from
direct rupture of intra-cerebral vessels at the time
of trauma.
DIFFUSE AXONAL INJURY
It occur in patient who have severe neurologic

67. .
CONTINUE……………………
impairment but don’t have massive grossly
visible brain damage. There is a diffuse
damage to white matter in the form of
ruptured axons. The patient is comatose.

68. TREATMENT
 Get plenty of sleep at night and rest during day
time
 Increase your activity slowly
 Avoid alcohol , drugs and caffeine
 Eat brain healthy foods
 Stay hydrated by drinking plenty of water
 Write down the things that may be harder than
usual for you to remember.

69. ENCEPHALITIS

70. ENCEPHALITIS
Encephalitis is the inflammation of brain.
TYPES
i. Viral Encephalitis
ii. Fungal Encephalitis
iii. Bacterial Encephalitis

71. VIRAL ENCEPHALITIS
Viral encephalitis is rare and usually associated
with a recent viral infection. Most cases are
associated with rabies or herpes simplex
virus.
Many different sites can be affected and as
neurones cannot be replaced , loss of function
reflects the extent of damage.
If vital centres in the medulla are involved the
condition can be fatal.

72. FUNGAL ENCEPHALITIS
Fungal infections of the CNS occur rarely in
healthy people. Causes of fungal infection include
Cryptococcus neoformans , Blastomyces
dermatitidis , Histoplasma capsulatum ,
Aspergillus fumigatus , Candida ,
Coccidioides immitis.
The presentation of fungal encephalitis is related to
geographic area or to immune system that is
compromised due to diseases or
immunosuppressive medication.

73. BACTERIAL
ENCEPHALITIS
It results from spread of infection from an
infected middle ear or paranasal sinuses or
secondary to trauma and pre-exisiting
meningitis.
The pure parenchymal infection occurs in
parenchymal forms of Tuberculosis and
Neurosyphilis.

74. SIGN AND SYMPTOMS
 Fever
 Seizures
 Headache
 Movement Disorder
 Sensitivity of light
 Sensitivity of sound
 Neck Stiffness
 Loss of consciousness

75. LAB TESTING
MRI
EEG
Blood Test- to check for the presence of
bacteria and viruses

76. NURSING MANAGEMENT
• Increased patient awareness and sensory
function
• Bed rest with supine sleeping position without a
pillow
• Monitor the signs of neurologic status with GCS
• Monitor vital signs
• Provide treatment in accordance with physician
advice
• Reduce the headache.

77. MEDICAL MANAGEMENT
• IV fluids to ensure proper hydration and levels
of essential minerals
• Anti-Inflammatory drugs such as
corticosteroids.
• Reduce swelling and pressure within skull
• Anticonvulsant medications such as phenytoin
to stop or prevent seizure.