Ammar Hyder

UNIT III: Disorders of Neurological System

A. Pain
THE SOMATOSENSORY SYSTEM
The somatosensory system relays information about four major
modalities: touch, temperature, body position, and pain.
Sensory neurons can be divided into three types that vary in
distribution:
 General somatic afferent neurons have branches with
widespread distribution throughout the body and with many
distinct types of receptors that result in sensations such as pain,
touch, and temperature.
 Special somatic afferent neurons have receptors located primarily in muscles, tendons, and
joints. These receptors sense position and movement of the body.
 General visceral afferent neurons have receptors on various visceral structures that sense
fullness and discomfort.
Somatosensory information is sequentially transmitted over three types of neurons:
 First-order neurons, which transmit information from sensory receptors to dorsal horn
neurons;
 Second-order CNS association neurons, which communicate with various reflex circuits and
transmit information to the thalamus;
 Third-order neurons, which forward the information from the thalamus to the sensory cortex.
Nociceptors
Nociceptors, or pain receptors, are sensory receptors that are activated by noxious insults to
peripheral tissues. These receptive endings, which are widely distributed in the skin, dental pulp,
periosteum, meninges, and some internal organs, translate the noxious stimuli into action
potentials that are transmitted by a dorsal root ganglion to the dorsal horn of the spinal cord.
Nociceptive action potentials are transmitted through two types of afferent nerve fibers:
 Myelinated Aδ fibers: Aδ fibers have considerably greater conduction velocities,
transmitting impulses at a rate of 6 to 30 m/second. Pain conducted by Aδ fibers traditionally
is called fast pain and typically is elicited by mechanical or thermal stimuli.
 Unmyelinated C fibers: C fibers are the smallest of all peripheral nerve fibers; they transmit
impulses at the rate of 0.5 to 2.0 m/second. C-fiber pain often is described as slow wave pain
because it is slower in onset and longer in duration. Elicits by persistent chemical or thermal
stimuli.

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ENDOGENOUS ANALGESIC MECHANISMS

There is evidence that opioid receptors and endogenously
synthesized opioid peptides, which are morphine-like
substances, are found on the peripheral processes of primary
afferent neurons and in many regions of the CNS
Three families of endogenous opioid peptides have been
identified—the enkephalins, endorphins, and dynorphins. Each
family is derived from a distinct precursor polypeptide and has a
characteristic anatomic distribution
Although the endogenous opioid peptides appear to function as
neurotransmitters, their full significance in pain control and other
physiologic functions is not completely understood.
Opioid agonists inhibit calcium channels in dorsal root and
trigeminal ganglion neurons as well as on primary afferent
neurons. Because it is calcium ions that cause neurotransmitter
release at the synapse, such calcium blockage would inhibit
synaptic transmission of pain impulses.
FIGURE • The path of the pain stimulus. (1) Pain begins as a message received by nerve
endings, such as in a burned finger. (2) The release of substance P, bradykinin, and
prostaglandins sensitize the nerve endings, helping to transmit the pain from the site of injury
toward the brain. (3) The pain signal then travels as an electrochemical impulse along the length
of the nerve to the dorsal horn on the spinal cord, a region that receives signals from all over the
body. (4) The spinal cord then sends the message to the thalamus and then to the cortex. (5) Pain
relief starts with signals from the brain that descend by way of the spinal cord, where (6)
chemicals such as endorphin S are released in the dorsal horn to diminish the pain message.
MECHANISM OF PAIN RELIEF ASSOCIATED WITH THE USE OF HEAT, COLD & TENS
HEAT

 Heat dilates blood vessels and increases local blood flow.

 It also can influence the transmission of pain impulses and increase collagen extensibility.
 An increase in local circulation can reduce the level of nociceptive stimulation by reducing
local ischemia caused by muscle spasm or tension, increase the removal of metabolites and
inflammatory mediators that act as nociceptive stimuli, and help to reduce swelling and
relieve pressure on local nociceptive endings.
 The heat sensation is carried to the posterior horn of the spinal cord and may exert its effect
by modulating projection of pain transmission.
 It also may trigger the release of endogenous opioids.
 Heat also alters the viscosity of collagen fibers in ligaments, tendons, and joint structures so
that they are more easily extended and can be stretched further before the nociceptive
endings are stimulated.

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 Thus, heat often is applied before therapy aimed at stretching joint structures and increasing
range of motion.
COLD
 Cold exerts its effect on pain through circulatory and neural mechanisms.
 The initial response to local application of cold is sudden local vasoconstriction.
 This initial vasoconstriction is followed by alternating periods of vasodilation and
vasoconstriction during which the body “hunts” for its normal level of blood flow to prevent
local tissue damage.
 The vasoconstriction is caused by local stimulation of sympathetic fibers and direct cooling
of blood vessels, and the hyperemia by local autoregulatory mechanisms.
 In situations of acute injury, cold is used to produce vasoconstriction and prevent
extravasation of blood into the tissues.
 Pain relief results from decreased swelling and decreased stimulation of nociceptive endings.
 The vasodilation that follows can be useful in removing substances that stimulate nociceptive
endings.
 Cold also can have a marked and dramatic effect on pain that results from the spasm-induced
accumulation of metabolites in muscle. In terms of pain modulation, cold may reduce
afferent activity reaching the posterior horn of the spinal cord by modulating sensory input.
TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION
TENS refers to the transmission of electrical energy across the surface of the skin to the
peripheral nerve fibers that stimulates nerve fibers to block the transmission of pain impulses to
the brain.
There probably is no single explanation for the physiologic effects of TENS. The gate control
theory was proposed as one possible mechanism:
 According to this theory, pain information is transmitted by small-diameter Aδ and C fibers.
 Large diameter afferent A fibers and small-diameter fibers carry tactile information mediating
touch, pressure, and kinesthesia.
 TENS may function on the basis of differential firing of impulses in the large fibers that carry
nonpainful information.
 Accordingly, increased activity in these larger fibers purportedly modulates transmission of
painful information to the forebrain.
 TENS has the advantage that it is noninvasive, easily regulated by the person or health
professional, and effective in some forms of acute and chronic pain.
B. Disorders of Neurological function
CEREBRAL CIRCULATION
Cerebral circulation is the movement of blood through a network of cerebral arteries and veins
supplying the brain.

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Blood supply
Blood supply to the brain is normally divided into anterior and
posterior segments, relating to the different arteries that supply the
brain. The two main pairs of arteries are the Internal carotid
arteries (supply the anterior brain) and vertebral arteries (supplying
the brainstem and posterior brain). The anterior and posterior
cerebral circulations are interconnected via bilateral posterior
communicating arteries. They are part of the Circle of Willis,
which provides backup circulation to the brain.
Anterior cerebral circulation
The ophthalmic artery and its branches.
The anterior cerebral circulation is the blood supply to the
anterior portion of the brain including eyes. It is supplied by the
following arteries:
 Internal carotid arteries: These large arteries are the medial branches of the common
carotid arteries which enter the skull, as opposed to the external carotid branches which
supply the facial tissues; the internal carotid artery branches into the anterior cerebral
artery and continues to form the middle cerebral artery.
 Anterior cerebral artery (ACA)
o Anterior communicating artery: Connects both
anterior cerebral arteries, within and along the floor
of the cerebral vault.
 Middle cerebral artery (MCA)
Posterior cerebral circulation
The anterior and posterior circulations meet at the Circle of Willis,
pictured here, which rests at the top of the brainstem. Inferior view.
The posterior cerebral circulation is the blood supply to the
posterior portion of the brain, including the occipital lobes, cerebellum and brainstem. It is
supplied by the following arteries:
 Vertebral arteries: These smaller arteries branch from the subclavian arteries which
primarily supply the shoulders, lateral chest, and arms. Within the cranium the two vertebral
arteries fuse into the basilar artery.
o Posterior inferior cerebellar artery (PICA)
 Basilar artery: Supplies the midbrain, cerebellum, and usually branches into the posterior
cerebral artery

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o Anterior inferior cerebellar artery (AICA)

o Pontine branches
o Superior cerebellar artery (SCA)
 Posterior cerebral artery (PCA)
 Posterior communicating artery
Venous drainage
The venous drainage of the cerebrum can be separated into two subdivisions: superficial and
deep.
The superficial system
The superficial system is composed of dural venous sinuses, sinuses (channels) within the dura
mater. The dural sinuses are therefore located on the surface of the cerebrum. The most
prominent of these sinuses is the superior sagittal sinus which is located in the sagittal plane
under the midline of the cerebral vault, posteriorly and inferiorly to the confluence of sinuses,
where the superficial drainage joins with the sinus that primarily drains the deep venous system.
From here, two transverse sinuses bifurcate and travel laterally and inferiorly in an S-shaped
curve that forms the sigmoid sinuses which go on to form the two jugular veins. In the neck,
the jugular veins parallel the upward course of the carotid arteries and drain blood into
the superior vena cava. The veins puncture the relevant dural sinus, piercing the arachnoid and
dura mater as bridging veins that drain their contents into the sinus.
The deep venous system
The deep venous system is primarily composed of traditional veins inside the deep structures of
the brain, which join behind the midbrain to form the great cerebral vein (vein of Galen). This
vein merges with the inferior sagittal sinus to form the straight sinus which then joins the
superficial venous system mentioned above at the confluence of sinuses.
BLOOD–BRAIN BARRIERS
The blood–brain barrier depends on the unique characteristics of the brain capillaries.
Endothelial cells of brain capillaries are joined by continuous tight junctions. In addition, most
brain capillaries are surrounded by a basement membrane and by the processes of supporting
cells of the brain, called astrocytes. The blood–brain barrier permits passage of essential
substances while excluding unwanted materials. Reverse transport systems remove materials
from the brain. Large molecules, such as proteins and peptides, are largely excluded from
crossing the blood–brain barrier
CEREBROSPINAL FLUID–BRAIN BARRIER
The ependymal cells covering the choroid plexus are linked together by tight junctions, forming
a blood–CSF barrier to diffusion of many molecules from the blood plasma of choroid plexus

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capillaries to the CSF. Water is transported through the choroid epithelial cells by osmosis.
Oxygen and carbon dioxide move into the CSF by diffusion, resulting in partial pressures
roughly equal to those of plasma. The high sodium and low potassium contents of the CSF are
actively regulated and kept relatively constant. Lipids and nonpeptide hormones diffuse through
the barrier rather easily, but most large molecules, such as proteins, peptides, many antibiotics,
and other medications, do not normally get through.
STROKE (BRAIN ATTACK)
Stroke is the syndrome of acute focal neurologic deficit from a vascular disorder that injures
brain tissue. There are two main types of strokes: ischemic and hemorrhagic.
 Ischemic strokes are caused by an interruption of blood flow in a cerebral vessel and are the
most common type of stroke, accounting for 87% of all strokes.
 Hemorrhagic strokes account for 13% of all strokes. A hemorrhagic stroke usually is from a
cerebral blood vessel rupture caused by hypertension, aneurysm, or arteriovenous
malformation and has a much higher fatality rate than ischemic strokes.
Risk factors
Nonmodifiable Factors Modifiable Factors Modifiable Behavioral Factors
 Age  Hypertension  Cigarette smoking
 Sex  Hypercholesteremia  Alcohol
 Race  Diabetes mellitus  Birth control pills
 Prior stroke  Hyper coagulopathy  Physical inactivity
 Family history  Cardiac disease  Obesity
 Illicit drug use

Ischemic Stroke
Classified into five main mechanisms of stroke subtypes and their frequency:
 20% large artery thrombosis (atherosclerotic disease),
 25% small penetrating artery thrombosis disease (lacunar stroke),
 20% cardiogenic embolism,
 30% cryptogenic stroke (undetermined cause), and 5% other
Ischemic Penumbra in Evolving Stroke. During the evolution of a stroke, there usually is a
central core of dead or dying cells, surrounded by an ischemic band or area of minimally
perfused cells called the penumbra (border zone). Brain cells of the penumbra receive marginal
blood flow, their metabolic activities are impaired, but the structural integrity of the brain cells is
maintained.
Large-Vessel (Thrombotic) Stroke. Thrombi are the most common cause of ischemic strokes,
usually occurring in atherosclerotic blood vessels. Common sites of plaque the internal carotid
and vertebral arteries, and junctions of the basilar and vertebral arteries. Cerebral infarction can
result from an acute local thrombosis and occlusion at the site of chronic atherosclerosis, with or

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without embolization of the plaque material distally, or from critical perfusion failure distal to a
stenosis (watershed)
Small-Vessel Stroke (Lacunar Infarct). Lacunar infarcts are small (1.5- to 2-cm) to very small
(3- to 4-mm) infarcts located in the deeper, noncortical parts of the brain or in the brain stem.
They are found in the territory of single deep penetrating arteries supplying the internal capsule,
basal ganglia, or brain stem. They result from occlusion of the smaller penetrating branches of
large cerebral arteries, commonly the middle cerebral and posterior cerebral arteries. Six basic
causes of lacunar infarcts have been proposed: embolism, hypertension, small-vessel occlusive
disease, hematologic abnormalities, small intracerebral hemorrhages, and vasospasm.
Cardiogenic Embolic Stroke. An embolic stroke is caused by a moving blood clot that travels
from its origin to the brain. It usually affects the larger proximal cerebral vessels, often lodging
at bifurcations. The most frequent site of embolic strokes is the middle cerebral artery, reflecting
the large territory of this vessel and its position as the terminus of the carotid artery. Although
most cerebral emboli originate from a thrombus in the left heart, they also may originate in an
atherosclerotic plaque in the carotid arteries. The embolus travels quickly to the brain and
becomes lodged in a smaller artery through which it cannot pass.
Transient Ischemic Attacks
 TIAs are a transient episode of neurological dysfunction caused by focal brain, spinal cord,
or retinal ischemia, without acute infarction.
 A TIA reflects a temporary disturbance in focal cerebral blood flow, which reverses before
infarction occurs.
 The causes of TIAs are the same as those of ischemic stroke and include atherosclerotic
disease of cerebral vessels and emboli.
 TIAs are important because they may provide warning of impending stroke.
 There is a higher risk of early stroke after TIA, 10% to 15% have a stroke within 3 months,
with 50% occurring in 48 hours.
 Diagnosis of TIA before a stroke may permit surgical or medical intervention that prevents
an eventual stroke and the associated neurologic deficits.
Hemorrhagic Stroke
 The most frequently fatal stroke results from the spontaneous rupture of a cerebral blood
vessel.
 The resulting intracerebral hemorrhage can cause a focal hematoma, edema, compression of
the brain contents, or spasm of the adjacent blood vessels.
 The most common predisposing factors are advancing age and hypertension.
 Other causes of hemorrhage are trauma, erosion of the vessels by tumors, blood coagulation
disorders, vasculitis, and drugs. Aneurysms and arteriovenous malformations are structural
abnormalities that can also cause sudden hemorrhage

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