GENERAL NEUROLOGY (Q.

1-37)
1) Reflexes classification, reflex arc, examination of normal reflexes.
A reflex is an involuntary and nearly instantaneous movement in response to a stimulus. A true
reflex is a behavior which is mediated via the reflex arc.
A reflex arc is a neural pathway that controls an action reflex. Most sensory neurons do not
pass directly into the brain, but synapse in the spinal cord. This characteristic allows reflex
actions to occur relatively quickly by activating spinal motor neurons without the delay of
routing signals through the brain, although the brain will receive sensory input while the reflex
action occurs. There are two types of reflex arc - autonomic reflex arc (affecting inner organs)
and somatic reflex arc (affecting muscles). Monosynaptic refers to the presence of a single
chemical synapse. In polysynaptic reflex pathways involve one or more interneurons
connect afferent (sensory) and efferent (motor) signals.
The most important reflexes in clinical diagnosis are the biceps (C5C6), brachioradialis (C5C6),
triceps (C7C8), adductor (L2L4), quadriceps (L2/3L4), posterior tibial (L5), and Achilles (S1
S2) reflexes. Some clinically important extrinsic reflexes are the abdominal (T6 T12),
cremasteric (L1L2), bulbocavernosus (S3 S4), and anal wink (S3S5) reflexes.
2) Reflexes quantitative changes, pathological reflexes.
A reflex action is an involuntary and nearly instantaneous movement in response to
a stimulus. A true reflex is a behavior which is mediated via the reflex arc.
Abnormal reflexes:
-Babinski sign: the plantar reflex is a reflex elicited when the sole of the foot is stimulated with
a blunt instrument. In normal adults the plantar reflex causes a downward response of
the hallux (flexion). An upward response (extension) of the hallux is known as Babinski
response. The Babinski sign can indicate upper motor neuron lesion constituting damage to
the corticospinal tract.
-Clonus is a series of involuntary muscular contractions and relaxations. Clonus is a sign of
certain neurological conditions and it is particularly associated with upper motor
neuron lesions such as in stroke, multiple sclerosis, spinal cord damage and hepatic
encephalopathy.Spontaneous twitching known as fasciculations usually caused by lower motor
neuron pathology, clonus causes large motions that are usually initiated by a reflex. Clonus is
most common in the ankles, where it is tested by rapidly flexing the foot upward. It can also be
tested in the knees by rapidly pushing the patella towards the toes.

-Hyperreflexia is defined as overactive or overresponsive reflexes. Examples of this can include

spastic tendencies, which are indicative of upper motor neuron disease as well as the lessening
or loss of control ordinarily exerted by higher brain centers of lower neural pathways. The most
common cause of hyperreflexia is spinal cord injury.
-Hyporeflexia is the condition of below normal or absent reflexes. Hyporeflexia is generally
associated with a lower motor neuron deficit at the alpha motor neurons from the spinal cord
to muscle.
3) Sensation anatomy, physiology of the superficial and deep sensibility.
Sensation:
The somatosensory system is a diverse sensory system composed of the receptors and
processing centres to produce the sensory modalities such as touch, temperature,
proprioception (body position), and nociception (pain). The sensory receptors cover the skin
and epithelia, skeletal muscles, bones and joints, internal organs, and the cardiovascular
system. The system reacts to diverse stimuli using different receptors: thermoreceptors,
nociceptors, mechanoreceptors and chemoreceptors. Transmission of information from the
receptors passes via sensory nerves through tracts in the spinal cord and into the brain.
Processing primarily occurs in the primary somatosensory area in the parietal lobe of the
cerebral cortex. The point-to-point mapping of the body surfaces in the brain is called a
homunculus and is essential in the creation of a body image. This brain-surface ("cortical") map
is not immutable. Dramatic shifts can occur in response to stroke or injury.
Superficial sensation: the awareness or perception of feelings in the superficial layers of the
skin in response to touch, pressure, temperature, and pain. Such sensations are conveyed to
the brain via the spinothalamic system.
Deep sensation: the awareness or perception of pain, pressure, or tension in the deep layers of
the skin, muscles, tendons, or joints. Such sensations are conveyed to the brain via the spinal
column.
General somatosensory pathway: a somatosensory pathway will typically have three long
neurons:

The first neuron always has its cell body in the dorsal root ganglion of the spinal nerve
(if sensation is in head or neck, it will be the trigeminal nerve ganglia or the ganglia of
other sensory cranial nerves).
The second neuron has its cell body either in the spinal cord or in the brainstem. This
neuron's ascending axons will cross to the opposite side either in the spinal cord or in
the brainstem. The axons of many of these neurones terminate in the thalamus, others
terminate in the reticular system or the cerebellum.
In the case of touch and certain types of pain, the third neuron has its cell body in the
thalamus and ends in the postcentral gyrus of the parietal lobe.

In the periphery, the somatosensory system detects various stimuli by sensory receptors (ex.
by mechanoreceptors for tactile sensation and nociceptors for pain sensation).
In the spinal cord, the somatosensory system includes ascending pathways from the body to
the brain. Some ascending pathways, particularly those involved with control of posture are
projected to the cerebellum.
In the brain, the primary somatosensory area in the human cortex is located in the
postcentral gyrus of the parietal lobe.
4) Sensation study of common sensation, sensory symptoms, sensory syndromes.
Human sensory system: consists of the following sub-systems:

Visual system consists of the photoreceptor cells, optic nerve, and V1.
Auditory system
Somatosensory system consists of the receptors, transmitters (pathways) leading to S1,
and S1 that experiences the sensations as touch or pressure, temperature (warm or
cold), pain (including itch and tickle), and the sensations of muscle movement and joint
position including posture, movement, and facial expression.
Gustatory system
Olfactory system

Sensory Symptoms:
Positive symptoms:

Pain
Hyperalgesia: when threshold to pain appears lowered.
Hyperpathia: pain threshold elevated, but once reached, the painful stimulus is
excessively felt.
Hyperaesthesia
Paraesthesia: burning feeling.
Dysaesthesia/allodynia: when touching is painful.
Neuralgia
Causalgia: spontaneous burning sensation with increased sensitivity to painful stimuli.
Phantom limb pain

Negative symptoms:

Hypaesthesia: decreased sensation.

Anaesthesia: loss of feeling.

Sensory Syndromes:
Peripheral Syndromes
Sensory Polyneuropathy, Diabetic Neuropathies, Acquired Immunodeficiency Syndrome
Associated Neuropathies, Toxic Neuropathies, Amyloid Neuropathy, Proximal Sensory Loss,
Temperature-Dependent Sensory Loss, Mononeuropathy.
Spinal Syndromes
Myelopathy, Syringomyelia, Spinal Hemisection.
Brain Syndromes
Thalamic Infarction and Hemorrhage, Thalamic Pain Syndrome, Trigeminal Neuralgia, Cortical
Infarction.
5) Pyramidal system. Examination of muscle strength. Lesion syndromes of the central and
peripheral motor neuron.
Pyramidal system: any of the important motor nerves on each side of the central nervous
system that run from the sensory motor areas of the cortex through the brainstem to motor
neurons of the cranial nerve nuclei and the ventral root of the spinal cord.
Muscle strength: the amount of force a muscle can produce with a single maximal effort. Size
of muscle cells and the ability of nerves to activate them are related to muscle strength. Upper
Extremity Strength Testing: Finger extension, Finger abduction, Thumb abduction in plane of
palm, Thumb abduction perpendicular to plane of palm, Thumb opposition, Wrist flexion and
hand abduction, Wrist extension and hand abduction, Elbow flexion, Elbow extension. Lower
Extremity Strength Testing: Hip flexion, Knee extension, Knee flexion, Leg abduction, Leg
adduction, Toe dorsiflexion, Foot dorsiflexion, Foot plantar flexion.
Upper motor neurons are motor neurons that originate in the motor region of the cerebral
cortex or the brain stem and carry motor information down to the final common pathway, that
is any motor neurons and they are not directly responsible for stimulating the target muscle.
The pyramidal tract is a collection of axons that travel between the cerebral cortex of
the brain and the spinal cord and mostly contains motor axons. It actually consists of two

separate tracts in the spinal cord: the lateral corticospinal tract and the anterior corticospinal
tract. The neurons of the corticospinal tracts are sometimes referred to as pyramidal tract
neurons (PTN), because their axons form part of the pyramidal tracts leading to the spinal cord.
Injuries to the motor pathways result in paralysis. Damage to the motor neurons in the frontal
cortex or their tracts result in upper motor neuron syndromes. For example, if the left lateral
corticospinal tract is damaged at the second cervical vertebra, control of the left upper and
lower limbs is lost. Upper motor neuron syndrome is characterized by spastic paralysis where
little atrophy of the muscle occurs. However uncoordinated hyper reflex activities where
muscle tone is increased, cause spastic movements where flexor and extensor alternately
contract. Injuries to the neurons in the vertebral horn of the cord result in a different type of
paralysis. Problems of this sort result in lower motor syndrome. Lower motor neuron syndrome
results in flaccid paralysis with loss of movement, tone and reflex activity. The muscle becomes
atrophied and flaccid.
6) Extrapyramidal system anatomy, physiology, extrapyramidal syndromes.
The extrapyramidal system includes all motor gray structures and pathways that are not
included in the pyramidal system. It is a set of subcortical circuits and pathways and includes
the basal ganglia, red nucleus, brain stem reticular formation and other brainstem nuclei.
-Extrapyramidal Structures:
*Cerebral cortex which are premotor frontal and cingulate gyrus.
*Basal ganglia
*Thalamus (ventral nuclei).
*Motor nuclei of the brainstem: -Red nucleus, -Reticular Formation of pons and medulla
oblongata, -Pontine nuclei, -Superior colliculi, -Lateral vestibular nucleus, -Inferior olive.
*Cerebellum
-Extrapyramidal Syndromes:
Parkinsonism is degeneration of the substantia nigra characterized
by tremor, hypokinesia, rigidity, and postural instability. The underlying causes of parkinsonism
are numerous, and diagnosis can be complex.
Chorea is nonrhythmic, jerky, rapid, nonsuppressible involuntary movements, mostly of distal
muscles or the face; movements may merge imperceptibly into purposeful or semipurposeful
acts that mask the involuntary movements.

Athetosis is nonrhythmic, slow, writhing, sinuous movements predominantly in distal muscles,

often alternating with postures of the proximal limbs to produce a continuous, flowing stream
of movement.
Hemiballismus is usually a unilateral, nonrhythmic, rapid, nonsuppressible, violent, flinging
movement of the proximal arm. Hemiballismus is caused by a lesion, usually an infarct, around
the contralateral subthalamic nucleus.
7) Muscle tone anatomy, physiology, examination of muscle tone, syndromes of disturbed
muscle tone.
Muscle tone is the continuous and passive partial contraction of the muscles, or the muscles
resistance to passive stretch during resting state. It helps maintain posture, and it declines
during sleep. Unconscious nerve impulses maintain the muscles in a partially contracted state.
If a sudden pull or stretch occurs, the body responds by automatically increasing the muscle's
tension, a reflex which helps guard against danger as well as helping to maintain balance.
Physical disorders can result in abnormally low (hypotonia) or high (hypertonia) muscle tone.
Another form of hypertonia is paratonia, which is associated with dementia.
-Hypotonia is seen in lower motor neuron disease like poliomyelitis. Hypotonia can present
clinically as muscle flaccidity, where the limbs appear floppy, stretch reflex responses are
decreased, and the limbs resistance to passive movement is also decreased.
-Hypertonia is seen in upper motor neuron diseases like lesions in pyramidal tract and
extrapyramidal tract. Hypertonia can present clinically as either spasticity or rigidity.
While spasticity is velocity-dependent resistance to passive stretch for example passively
moving an elbow quickly will elicit increased muscle tone, but passively moving elbow slowly
may not elicit increased muscle tone, rigidity is velocity-independent resistance to passive
stretch for example there is uniform increased tone whether the elbow is passively moved
quickly or slowly. Spasticity can be in the form of the clasp-knife response, in which there is
increased resistance only at the beginning or at the end of the movement. Rigidity can be the
leadpipe type in which there is resistance throughout to passive movement, or it may be of
cogwheel type in which the resistance to passive movement is in a jerky manner.
8) Cerebellum anatomy, physiology, cerebellar symptoms and syndromes.
The cerebellum is a region of the brain that plays an important role in motor control. It is also
involved in some cognitive functions such as attention and language. The cerebellum does not
initiate movement, but it contributes to coordination, precision, and accurate timing. It receives
input from sensory systems and from other parts of the brain and spinal cord, and integrates
these inputs to fine tune motor activity. In terms of anatomy, the cerebellum has the

appearance of a separate structure attached to the bottom of the brain, tucked underneath
the cerebral hemispheres. The surface of the cerebellum is covered with finely spaced parallel
grooves, in striking contrast to the broad irregular convolutions of the cerebral cortex. These
parallel grooves conceal the fact that the cerebellum is actually a continuous thin layer
of neural tissue, tightly folded in the style of an accordion. Within this thin layer are several
types of neurons with a highly regular arrangement, the most important being Purkinje
cells and granule cells. This complex neural network gives rise to a massive signal-processing
capability, but almost all of its output is directed to a set of small deep cerebellar nuclei lying in
the interior of the cerebellum. The signs and symptoms of cerebellar dysfunctions are
dysmetria, dysarthria, asynergia, nystagmus, ataxia, staggering gait, and adiadochokinesia.
Dysmetria refers to a lack of coordination of movement typified by undershoot or overshoot of
intended position with the hand, arm, leg, or eye.
Dysarthria is a motor speech disorder resulting from neurological injury of the motor
component of the motor-speech system and is characterized by poor articulation. Any of the
speech subsystemscan be affected, leading to impairments in intelligibility, audibility,
naturalness, and efficiency of vocal communication.
Asynergy is defective or lack of co-ordination between organs, muscles, limbs or joints,
resulting in a loss in movement or speed. Asynergy is most likely to occur during complex
movements, where several individual muscle contractions are needed to act in unison.
Asynergy may be caused by cerebellar disorders.
Nystagmus means involuntary eye movement.
The term cerebellar ataxia is used to indicate ataxia that is due to dysfunction of the
cerebellum. This causes a variety of elementary neurological deficits, such as
antagonist hypotonia, asynergy, dysmetria, dyschronometria, and dysdiadochokinesia.
9) Coordination of movements anatomy, physiology, examination, coordination syndromes.
Coordination of movements: the combination of body movements that result in intended
actions. Motor coordination is achieved when subsequent parts of the same movement, or the
movements of several limbs or body parts are combined in a manner that is well timed,
smooth, and efficient with respect to the intended goal. This involves the integration of
proprioceptive information detailing the position and movement of the musculoskeletal system
with the neural processes in the brain and spinal cord which control, plan, and relay motor
commands. The cerebellum plays a critical role in this neural control of movement and damage
to this part of the brain or its connecting structures and pathways results in impairment of
coordination, known as ataxia. Reaching for a pencil, grasping a doorknob, skiing, and tightrope

walkingto name but a few physical actionsall involve well-coordinated movements made
with well-balanced postures.
Coordination syndromes:
Severe alcoholism can lead to atrophy of the anterior lobe of the cerebellum and difficulty
walking. Parkinsons disease involves loss of dopamine-producing neurons in the substantia
nigra; it creates a variety of movement abnormalities such as akinesia (difficulty in initiating
movement), rigidity, and tremor. Widespread cortical atrophy and a variety of motor defects
characterize Alzheimers disease. Disorders of coordination and balance are more commonly
the result of cerebellar damage. These diseases can interfere with the fine-tuning of muscular
movement and result in coarse, uncoordinated movement. This type of condition is
called ataxia and is easily seen in a persons unsteady gait. A very different class of motor
abnormality comprises involuntary movements that a person cannot stop. These include:rather innocuous tics - low, writhing, well-coordinated movements of the arm - rhythmic
movements of the fingers - involuntary movements of the face and mouth - wildly violent,
throwing arm movements. Characteristically, almost all of these abnormal movements are the
result of problems in the normal functioning of the basal ganglia. Finally another motor
disorder, called dystonia, shows up as a continuous contraction of certain muscle groups,
resulting in steady, strange, abnormal postures.
10) Gait, synkinesias, speech and their disorders.
Gait is the way locomotion is achieved using human limbs. Different gaits are characterized by
differences in limb movement patterns, overall velocity, forces, kinetic and potential energy
cycles, and changes in the contact with the surface.
-Propulsive gait: in Parkinson's disease.
-Spastic (scissors) gait: in Brain abscess, Cerebrovascular accident (stroke), Multiple sclerosis,
Spinal cord trauma.
-Steppage gait: in Multiple sclerosis, Peroneal neuropathy.
-Waddling gait: in Muscular dystrophy, Muscle disease (myopathy), Spinal muscle atrophy.
-Ataxic gait: in Acute cerebellar ataxia, Alcohol intoxication, Polyneuropathy (damage to many
nerves, as occurs with diabetes).
Synkinesis is the result from miswiring of nerves after trauma. This result is manifested
through involuntary muscular movements accompanying voluntary movements. Almost all
cases of synkinesis develop as a sequel to nerve trauma. Trauma to the nerve can be induced in

cases such as surgical procedures, nerve inflammation, neuroma, and physical injury. The two
cases of synkinesis most commonly studied involve the facial muscles and the extraocular
muscles. Facial synkinesis is a common sequelae to Idiopathic Facial Nerve Paralysis which
occurs due to the compression of the seventh cranial nerve, results in a hemifacial paralysis due
to non-functionality of the nerve. As the nerve attempts to recover, nerve miswiring results.
The most common symptoms of facial synkinesis include: - eye closure with volitional
contraction of mouth muscles, - neck tightness, - hyperlacrimation. The six muscles around the
eye (extraocular muscles) are innervated by three different cranial nerves: Abducens (6th
nerve), Trochlear (4th nerve), and Oculomotor (3rd nerve). After nerve trauma around the eye,
a combination of any two of these three cranial nerves have been shown to be involved with
extra-ocular synkinesis.
Speech: Two areas of the cerebral cortex are necessary for speech. First is in the frontal lobe,
usually on the left, near the motor cortex controlling muscles of the lips, jaws, soft palate and
vocal cords. When damaged by a stroke or injury, comprehension is unaffected but speech is
slow. Secondly Wernicke's area lies to the back of the temporal lobe, again, usually on the left,
near the areas receiving auditory and visual information. Dysarthria is a weakness or paralysis
of speech muscles caused by damage to the nerves and/or brain. Aphasia - no speech.
11) Optic nerve anatomy, physiology, examination, syndromes.
The optic nerve transmits visual information from the retina to the brain.
Anatomy-Physiology: the fibres are covered with myelin produced by oligodendrocytes, rather
than Schwann cells, which are found in the peripheral nervous system, and are encased within
the meninges. The optic nerve is ensheathed in all three meningeal layers rather than
the epineurium, perineurium, and endoneurium found in peripheral nerves. The optic nerve is
composed of retinal ganglion cell axons and support cells. It leaves the orbit via the optic canal,
running postero-medially towards the optic chiasm, where there is a partial crossing of fibres
from the nasal visual fields of both eyes. Most of the axons of the optic nerve terminate in
the lateral geniculate nucleus from where information is relayed to the visual cortex, while
other axons terminate in the pretectal nucleus and are involved in reflexive eye movements.
Other axons terminate in the suprachiasmatic nucleus. The eye's blind spot is a result of the
absence of photoreceptors in the area of the retina where the optic nerve leaves the eye. Each
optic nerve contains around 1.2 million nerve fibers, which are axons of the retinal ganglion
cells of one retina. In the fovea, which has high acuity, these ganglion cells connect to as few as
5 photoreceptor cells; in other areas of retina, they connect to many thousand photoreceptors.
Syndromes: Damage to the optic nerve typically causes permanent and potentially severe loss
of vision, as well as an abnormal pupillary reflex. In general: Damage proximal to the optic

chiasm causes loss of vision in the visual field of the same side only. Damage in the chiasm
causes loss of vision laterally in both visual fields. Damage distal to the chiasm causes loss of
vision in one eye but affecting both visual fields. Injury to the optic nerve can be the result of
congenital problems. Most commanly Glaucoma is a group of diseases involving loss of
retinal ganglion cells causing optic neuropathy in a pattern of peripheral vision loss, initially
sparing central vision. Optic neuritis is inflammation of the optic nerve. It is associated with a
number of diseases; the most notable is multiple sclerosis. Anterior Ischemic Optic
Neuropathy is a particular type of infarct that affects patients with an anatomical
predisposition and cardiovascular risk factors. Optic nerve hypoplasia is the underdevelopment of the optic nerve causing little to no vision in the affected eye.
12) Oculo-motor cranial nerves, anatomy, physiology, examination, syndromes.
The oculomotor nerve controls most of the eye's movement and constriction of the pupil, and
maintains an open eyelid. The oculomotor nerve (CN III) arises from the anterior aspect
of mesencephalon (midbrain). There are two nuclei for the oculomotor nerve: The oculomotor
nucleus originates at the level of the superior colliculus and The Edinger-Westphal
nucleus supplies parasympathetic fibres to the eye via the ciliary ganglion.
The trochlear nerve is a motor nerve that innervates a single muscle: the superior
oblique muscle of the eye. The trochlear nerve emerges from the dorsal aspect of the
brainstem at the level of the caudalmesencephalon, just below the inferior colliculus. It circles
anteriorly around the brainstem and runs forward toward the eye in the subarachnoid space. It
passes between the posterior cerebral artery and the superior cerebellar artery.
The abducens nerve is a somatic efferent nerve that controls the movement of a single
muscle, the lateral rectus muscle of the eye. The abducens nerve leaves the brainstem at the
junction of the pons and the medulla, medial to the facial nerve. In order to reach the eye, it
runs upward (superiorly) and then bends forward (anteriorly).
Examination and Syndromes: ptosis, strabismus (crossed eyes) converge and divergent,
enopthalmus (recession f the eyeballs within the orbit), exopthalmus (protrusion of one or both
eyeballs), diplopia, nystagmus (rhythmic oscillation of the eyeballs), miosis (constriction of the
pupil), mydriasis (dilatation of the pupil), anisocoria (two pupils are not of equal size),
opthalmoplegia (paralysis of one or more ocular muscles).
13) Olfaction and taste anatomy, physiology, examination, syndromes.
Olfaction is the sense of smell. This sense is mediated by specialized sensory cells of the nasal
cavity of vertebrates and sensory cells of the antennae of invertebrates. Many vertebrates have
two distinct olfactory systemsthe main olfactory system and the accessory olfactory

system.The main olfactory system detects volatile chemicals and the accessory olfactory system
detects fluid-phase chemicals.The chemicals are present in the surrounding aqueous medium.
Olfaction is a form of chemoreception. The chemicals themselves activate the olfactory system
generally at very low concentrations so they are called odorants.
Syndromes: Anosmia inability to smell, Cacosmia things smell like feces, Dysosmia things
smell different than they should, Hyperosmia an abnormally acute sense of smell.
Hyposmia decreased ability to smell. Olfactory reference syndrome is a psychiatric
condition in which the affected person is excessively preoccupied by the concern that
one's body odor is foul or unpleasant.
Taste refers to the ability to detect the flavor of substances such as food. Humans receive tastes
through sensory organs called taste buds. It is concentrated on the upper surface of
the tongue. Disorders of taste are ageusia and dysgeusia. Ageusia is the loss of taste functions
of the tongue. Tissue damage to the nerves that support the tongue can cause ageusia,
especially damage to the lingual nerve and the glossopharyngeal nerve. Dysgeusia is the
distortion of the sense of taste. Hypogeusia is a reduced ability to taste things.
14) Trigeminal nerve anatomy, physiology, examination, syndromes.
The trigeminal nerve is responsible for sensation in the face. Sensory information from the face
and body is processed by parallel pathways in the central nervous system. The fifth nerve is
primarily a sensory nerve, but it also has certain motor functions. The sensory function of the
trigeminal nerve is to provide the tactile, proprioceptive, and nociceptive afference of the face
and mouth. The motor function activates the muscles of mastication, the tensor
tympani, tensor veli palatini, mylohyoid, and anterior belly of the digastric. It has three
branches. The ophthalmic nerve (V1) carries sensory information from the scalp and forehead,
the maxillary nerve (V2) carries sensory information from the lower eyelid and cheek,
the mandibular nerve (V3) carries sensory information from the lower lip.
Syndromes: Trigeminal neuralgia is aneuropathic disorder characterized by episodes of
intense pain in the face, originating from the trigeminal nerve. The disorder is characterized by
episodes of intense facial pain that last from a few seconds to several minutes or hours. The
episodes of intense pain may occur paroxysmally. It can be caused by irritation of the nerve as it
enters the brainstem itself for example by multiple sclerosis. Abnormal paroxysmal discharges
within the nerve give rise to the lancinating pain. Herpes zoster affects also the trigeminal
nevre. Though the virus is in the trigeminal ganglion, clinical involvement is most usually
confined to the skin and cornea supplied by the ophthalmic branch.
15) Facial nerve anatomy, physiology, examination, syndromes.

The facial nerve leaves the pons in the cerebellopontine angle. It provides autonomic efferent
fibres to lacrimal and salivary glands, collects afferent taste fibres from the anterior two-thirds
of the tongue and it provides the innervation of the stapedius muscle in the ear, before
emerging from the stylomastoid foramen behind and below the ear to innervate the facial
muscles.
Syndromes: Bell's palsy is a form of facial paralysis resulting from a dysfunction of the facial
nerve that results in the inability to control facial muscles on the affected side. Several
conditions can cause facial paralysis, brain tumor, stroke, and Lyme disease. Bell's palsy is the
most common acute mononeuropathy. Hemifacial spasm: brief spontaneous twitches.
Peripheral paralysis: loss of facial nerve function.
16) Auditory vestibular nerve anatomy, physiology, examination, syndromes.
The vestibulocochlear nerve is responsible for transmitting sound and equilibrium information
from the inner ear to the brain. This is the nerve along which the sensory cells of the inner
ear transmit information to the brain. It consists of the cochlear nerve, carrying information
about hearing, and the vestibular nerve, carrying information about balance. It emerges from
the pons and exits the inner skull via the internal acoustic meatus in the temporal bone. The
vestibulocochlear nerve consists mostly of bipolar neurons and splits into two large divisions:
the cochlear nerve and the vestibular nerve.
Syndromes: Damage to the vestibulocochlear nerve: hearing loss (deafness), vertigo , false
sense of motion, loss of equilibrium, nystagmus, and sensation of noises in the ear (tinnitus).
Acoustic neuroma is an occasional cause of slowly progressive unilateral nerve deafness. The
tumour is a benign one, derived from the Schwann cells on the 8th nerve. The common
diseases to affect balance without hearing loss can be seen that the lesion is likely to be central
in the brainstem, or peripheral in the labyrinth. The commonest type of severe vertigo is due to
sudden vestibular failure. This denotes the sudden occurrence of rotatory vertigo, gait ataxia,
vomiting and the need to stay in bed. Lateralized nystagmus and gait ataxia are the two
abnormal physical signs.
17) Bulbar cranial nerves. Bulbar and pseudobulbar paresis.
Bulbar cranial nerves: Glossopharyngeal (IX), Vagus (X), Accessory (XI) and Hypoglossal (XII).
Together they innervate the mouth and throat for normal speech and swallowing. They are
commonly involved in disease processes together to give rise to the clinical picture of bulbar
palsy. The glossopharyngeal nerve supplies the palate and pharynx, the vagus nerve supplies
the pharynx and larynx, and the hypoglossal nerve supplies the tongue. Taste perception in the
posterior third of the tongue is a function of the glossopharyngeal nerve. Both the
glossopharyngeal and vagus nerves have an enormous autonomic function. Innervation of the

vocal cords by the long, thin, recurrent laryngeal nerves exposes them to possible damage as
far down as the subclavian artery on the right, and the arch of the aorta on the left. Bulbar
palsy: when there is bilateral impairment of function in the 9th, 10th and 12th cranial nerves,
the clinical syndrome of bulbar palsy envolves.
The features of bulbar palsy are:
-dysarthria,
-dysphagia, often with choking episodes and/or nasal regurgitation of fluids,
-dysphonia and poor cough.
When motor neurone disease is causing loss of motor neurones from the lower cranial motor
nuclei in the medulla, the bulbar palsy can eventually lead to extreme difficulty in speech and
swallowing. Myasthenia gravis: bulbar muscle involvement in myasthenia gravis is quite
common in this rare condition. The fatiguability of muscle function, which typifies myasthenia,
is frequently very noticeable in the patients speech and swallowing. The speech disturbance in
patients with dysarthria is a purely mechanical one caused by defective movement of the lips,
tongue, palate, pharynx and larynx.
18) Gnosis and agnosia.
Gnosis: perceptive faculty enabling to perform very complex analysis of the sensory
information recognition and identification of the objects.
Agnosia is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the
specific sense is not defective nor is there any significant memory loss. It is usually associated
with brain injury or neurological illness, particularly after damage to the occipitotemporal
border, which is part of the ventral stream. Agnosia can result from strokes, dementia, or
other neurological disorders. It may also be trauma-induced by a head injury, brain infection, or
hereditary. Patients may improve if information is presented in other modalities than the
damaged one. There is no cure. Occupational therapy or speech therapy can improve agnosia,
depending on its etiology.
19) Praxis and apraxia.
Praxis: the ability to plan and correctly smoothly and automatically perform purposeful motor
acts.
Apraxia is a disorder caused by damage to specific areas of the cerebrum. Apraxia is
characterized by loss of the ability to execute or carry out learned purposeful movements,
despite having the desire and the physical ability to perform the movements. It is a disorder of

motor planning, which may be acquired or developmental, but may not be caused by
incoordination, sensory loss, or failure to comprehend simple commands .There are many
different forms of apraxia. Some of them are: Ideomotor apraxia - loss of ability to voluntarily
perform a learned task when given the necessary objects and Limb-kinetic apraxia - difficulty
making precise movements with an arm or leg, Verbal apraxia - trouble coordinating mouth
movements and speech. Recommended treatment for individuals with apraxia includes physical
therapy, occupational therapy.
20) Dysfunctions of speech. Aphasia.
Aphasia is an impairment of language ability. This class of language disorder ranges from having
difficulty remembering words to being completely unable to speak, read, or write. Aphasia
disorders usually develop quickly as a result of stroke, but can develop slowly from a brain
tumor, infection or can be a learning disability such as dysnomia. The area and extent of brain
damage determine the type of aphasia and its symptoms. Aphasia usually results
from lesions to the language-relevant areas of the frontal, temporal and parietal lobes of the
brain. These areas are almost always located in the left hemisphere, and in most people this is
where the ability to produce and comprehend language is found. Aphasia may also develop
slowly and it may also be caused by a sudden hemorrhagic event within the brain. Certain
chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia
as an episodic symptom. There is no one treatment proven to be effective for all types of
aphasias. Sings and sympthoms are inability to comprehend language, inability to pronounce,
inability to speak, poor enunciation, inability to read, inability to write, inability to repeat a
phrase.
21) Reticular formation anatomy, physiology. Sleep and waking and their disturbances.
The reticular formation is a part of the brain that is involved in actions such as
awaking/sleeping cycle, and filtering incoming stimuli to discriminate irrelevant background
stimuli. The reticular formation consists of more than 100 small neural networks, with varied
functions including: 1. Somatic motor control, 2. Cardiovascular control, 3. Pain modulation, 4.
Sleep and consciousness, 5. Habituation.
Sleep is a naturally recurring state characterized by reduced or absent consciousness, relatively
suspended sensory activity, and inactivity of nearly all voluntary muscles. Sleep is divided into
two broad types: rapid eye movement and non-rapid eye movement sleep. Sleep stages and
other characteristics of sleep are commonly assessed by polysomnography in a specialized
sleep laboratory. Measurements taken include EEG of brain waves, electrooculography of eye
movements, and electromyography of skeletal muscle activity.

A sleep disorder is a medical disorder of the sleep patterns of a person. Primary insomnia:
Chronic difficulty in falling asleep and/or maintaining sleep when no other cause is found for
these symptoms. Delayed sleep phase syndrome: inability to awaken and fall asleep at socially
acceptable times but no problem with sleep maintenance. Hypopnea syndrome: Abnormally
shallow breathing or slow respiratory rate while sleeping. Somniphobia: a dread of sleep.
Cataplexy: a sudden weakness in the motor muscles that can result in collapse to the floor.
Sleep paralysis: is characterized by temporary paralysis of the body shortly before or after
sleep. Sleep paralysis may be accompanied by visual, auditory.
22) Consciousness qualitative and quantitative disorders. Brain death.
Conciousness derives from a need to treat people whose brain function has been impaired as a
result of disease, brain damage, toxins, or drugs. Consciousness is assessed as a "level" ranging
from coma and brain death at the low end, to full alertness and purposeful responsiveness at
the high end. Consciousness is examined using a set of procedures known
as neuropsychological assessment. There are two commonly used methods for assessing the
level of consciousness of a patient: a simple procedure that requires minimal training, and a
more complex procedure that requires substantial expertise. The simple procedure begins by
asking whether the patient is able to move and react to physical stimuli. The next question is
whether the patient can respond in a meaningful way to questions and commands; patient is
asked for name, current location, and current day and time. A patient who can answer all of
these questions is usually considered fully conscious. The more complex procedure is known as
a neurological examination. A formal neurological examination runs through a precisely
delineated series of tests, beginning with tests for basic sensor motor reflexes, and culminating
with tests for sophisticated use of language. The outcome may be summarized using
the Glasgow Coma Scale. So it has three subscales, measuring the best motor response,
the best eye response and the best verbal response.
Disorders of consciousness: Minimally conscious state: is the patient has intermittent periods
of awareness and wakefulness and displays some meaningful behavior. Persistent vegetative
state: the patient has sleep-wake cycles, but lacks awareness and only displays reflexive and
non-purposeful behavior.
Brain death is the irreversible end of all brain activity due to total necrosis of the
cerebral neurons following loss of brain oxygenation. A brain-dead individual has no clinical
evidence of brain function upon physical examination. This includes no response to pain and
no cranial nerve reflexes. Reflexes include pupillary response, oculocephalic reflex, corneal
reflex, no response to the caloric reflex test and no spontaneous respirations.
23) Limbic system anatomy, physiology. Limbic disorders.

The limbic system is a set of brain structures including the hippocampus, amygdala, anterior
thalamic nuclei, septum, limbic cortex and fornix, which support a variety of functions including
emotion, behavior , long term memory, and olfaction. The limbic system is the set
of brain structures that forms the inner border of the cortex. The limbic system includes many
structures in the cerebral pre-cortex and sub-cortex of the brain. Hippocambus belongs to
the limbic system and plays important roles in the consolidation of information from short-term
memory to long-term memory and spatial navigation. The amygdalae are almond-shaped
groups of nuclei located deep within the medial temporal lobes of the brain and a primary role
in the processing and memory ofemotional reactions. The anterior nuclei of thalamus are
collection of nuclei at the rostral end of the dorsal thalamus.these nuclei are involved
in learning and memory. The septum pellucidum is a thin, triangular, vertical membrane
separating the anterior horns of the left and right lateral ventricles of the brain. The limbic
lobe is an arc-shaped region of cortex on the medial surface of each cerebral hemisphere of the
mammalian brain, consisting of parts of the frontal, parietal and temporal lobes.
Limbic disorders: Damage to the structures of limbic system results in conditions like:
Alzheimer's disease, anterograde amnesia, retrograde amnesia, and Kluver-Bucy syndrome.
24) Autonomic nervous system anatomy, physiology, clinical examination. Autonomic
visceral sensation.
The autonomic nervous system (ANS) is the part of the peripheral nervous system that acts as
a control system functioning largely below the level of consciousness, and
controls visceral functions. The ANS affects heart rate, digestion, respiration
rate, salivation, perspiration, diameter of the pupils. ANS innervation is divided
into sympathetic nervous system and parasympathetic nervous system divisions. The
sympathetic division has thoracolumbar of the spinal cord. The parasympathetic division has
craniosacral of spinal cord.
The autonomic nervous system (visceral,vegetative, involuntary) regulates the activities of the
visceral organs and maintains the homeostasis.
A.CENTRAL AUTONOMIC STRUCTURES: spinal cord, brainstem, hypothalamus, limbic system.
B.PERIPHERAL AUTONOMIC STRUCTURES: autonomic ganglia, autonomic plexuses
C.AUTONOMIC NEURONS: medial size, round pearlike vesicular form, two or more nuclei, poor
myelination of axons.
D.AUTONOMIC REFLEX ARC: Interoreceptors: mechano-, chemo-, osmo-, pain receptors.
Methods for investigation of the ANS:

A. Cardiovascular:
Measurement of heart rate and blood pressure before and after application of different stimuli.
Passive or active standing (orthoststic test)
Expiration against resistance after deep inspiration (test of Valsalva)
Deep breatning (respiratory arrhythmia)
Cold pressor test
Tonic muscle contraction (dynamic test)
Time-domain analysis of the heart rate /R-R intervals on the ECG/ and blood pressure,
evaluation of the autonomic balance
B. Investigation of the pupil functions
Direct or indirect pupil light reflex
C. Investigation of the lacrimal function
Schirmer`s test
D. Investigation of thermoregulatory and sudomotor functions
Thermoregulatory test
Sympathetic skin response
E. Investigation of the gastrointestinal, bladder and sexual functions
Investigation of the stomach emptying
Urofluometry
Measurement of residual urine
Sphincter EMG, EMG of corpus cavernosus
F. Pharmacological tests
Infusion of norepinephrine, angiotensine II, administration of atropin, ephedrine, neostygmine.
25) Autonomic syndromes. Pelvic autonomic regulation of reservoirs and sexual organs,
lesion syndromes.
Dysautonomia is a broad term that describes any disease or malfunction of the autonomic
nervous system. This includes postural orthostatic tachycardia syndrome, inappropriate sinus
tachycardia, vasovagal syncope, mitral valve prolapse dysautonomia, pure autonomic
failure, neurocardiogenic syncope, neurally mediated hypotension. The primary symptoms that
present in patients with dysautonomia are: Excessive fatigue, Excessive thirst (polydipsia),
dizziness, Feelings of anxiety, Rapid heart rate or slow heart rate, Orthostatic hypotension,
sometimes resulting in syncope. Causes of dysautonomias are: Autoimmune disorders, Brain
injury, Degenerative neurological diseases such as Parkinson's disease, Genetic factors, The
urinary bladder stores (continence) and voids (micturition) the urine produced by the kidneys.

Parasympathetic fibers arising in segments S2S4 and traveling through the pelvic plexus
activate the detrusor muscle of the bladder. Sympathetic fibers arising from segments T10 L2
and traveling through the hypogastric plexus inhibit the detrusor and stimulate the vesical neck.
Somatic motor impulses arising from segments S2S4 travel through the pudendal nerve to the
external sphincter and the pelvic floor muscles. Somatosensory fibers from the bladder travel
along the hypogastric and pelvic nerves to spinal levels T10L2 and S2S4, conveying
information about the state of bladder stretch. The central nervous system subserves the
voluntary inhibition of detrusor contraction. Neurogenic bladder dysfunction: useful diagnostic
aids include laboratory testing ultrasound examination ofkidney, bladder, pelvis, urodynamic
testing, micturition cystourethrography, and neurophysiological studies.
Sexual Function: The genital organs receive sympathetic, parasympathetic somatic motor and
somatosensory innervation and are under supraspinal control,mostly through hypothalamic
projections to the spinal cord. Hormonal factors also play an important role. Neurological
disease often causes sexual dysfunction in combination with bladder dysfunction. Isolated
sexual dysfunction is more often due to psychological factors, diabetes mellitus, endocrine
disorders, and atherosclerosis.
26) Hypothalamus anatomy, physiology, hypothalamic syndromes.
The hypothalamus lies in the anterior portion of the diencephalon, below the thalamus and
above the pituitary gland. It forms part of the wall and floor of the third ventricle. Among its
anatomical components are the preoptic area, infundibulum, tuber cinereum, and mamillary
bodies. It is responsible for the control and integration of endocrine function, hermoregulation
food intake, thirst, cardiovascular function, respiration, sexual function, behavior and memory,
and the sleepwake rhythm. Under the influence of changes in the external and internal
environment, and the emotional state of the individual, the hypothalamus controls the activity
of the ANS. The neuroendocrine control circuits of the hypothalamic-pituitary axis regulate the
plasma concentration of numerous hormones. Various regulatory hormones are secreted by
hypothalamic neurons into a local vascular network, through which they reach the
adenohypophysis to regulate the secretion of pituitary hormones into the systemic circulation.
A subset of hypothalamic neurons projects axons to the neurohypophysis. The bulblike endings
of these axons store oxytocin and antidiuretic hormone and secrete them directly into the
bloodstream. These hormones act directly on their effector organs. The ensuing effects are
sensed by the hypothalamus, thus closing the regulatory loop.
Syndromes: The majority of space-occupying lesions in the region of the pituitary are
adenomas. They are either non-adenomatous pituitary 'tumors', or are hypothalamic lesions. In
the case of a hypothalamic lesion, problems with appetite, thirst control and short-term
memory can be therapeutically highly problematic. Apart from craniopharyngiomas, the most

common abnormality is a Rathke's cleft cyst, which appears to be a developmental abnormality

which has a characteristic histology arachnoid cysts are not dissimilar, but contain CSF-like fluid
within a layer of epithelium. Both are usually treated surgically, with cystic components
sometimes requiring marsupialisation to prevent fluid reaccumulation, meningiomas and
astrocytomas are other intra-cranial lesion s which may present with hypothalamic syndromes;
meningiomas often have a characteristic radiological appearance, while optic nerve and
pilocytic gliomas are relatively benign.
27) CSF system and blood-brain barrier. Lumbar puncture. Examination of CSF. CSF
syndromes.
The ventricular system is a set of structures containing cerebrospinal fluid in the brain. It is
continuous with the central canal of the spinal cord. The system comprises four ventricles: right
and left lateral ventricles, third ventricle, and fourth ventricle. There are several small
holes that connect these ventricles, though only the first two of the list below are generally
considered part of the ventricular system. The bloodbrain barrier is a separation of
circulating blood and the brain extracellular fluid in the central nervous system. It occurs along
all capillaries and consists of tight junctions around the capillaries that do not exist in normal
normal.
Diseases involving the bloodbrain barrier are: Meningitis is an inflammation of the
membranes that surround the brain and spinal cord. Meningitis is most commonly caused by
infections with various pathogens, examples of which are Streptococcus
pneumoniae and Haemophilus influenzae. Epilepsy is a common neurological disease that is
characterized by recurrent and sometimes untreatable seizures. Several clinical and
experimental data have implicated the failure of bloodbrain barrier function in triggering
chronic or acute seizures, some studies implicate the interactions between a common blood
proteinalbumin and astrocytes. A lumbar puncture is a diagnostic and therapeutic procedure
that is performed in order to collect a sample of cerebrospinal fluid for biochemical,
microbiological and cytological analysis. Slit Ventricle Syndrome occurs in minority of patients
who have been shunted. Symptoms can include headache, varying degrees of lethargy, with or
without nausea, and vomiting.
28) Electroencephalography. Evoked potentials.
Electroencephalography is the recording of electrical activity along the scalp. EEG measures
voltage fluctuations resulting from ionic current flows within the neurons of the brain. EEG
refers to the recording of the brain's spontaneous electrical activity over a short period of time,
usually 2040 minutes, as recorded from multiple electrodes placed on the scalp. The main
diagnostic application of EEG is in the case of epilepsy, as epileptic activity can create clear

abnormalities on a standard EEG study. A secondary clinical use of EEG is in the diagnosis
of coma, encephalopathies, and brain death. EEG used to be a first-line method for the
diagnosis of tumors, stroke and other focal brain disorders. Routine EEG is typically used in the
following clinical circumstances: to distinguish epileptic seizures from other types of spells, to
serve as an adjunct test of brain death.
An evoked potential is an electrical potential recorded from the nervous system of a human
following presentation of a stimulus, as distinct from spontaneous potentials as detected
by electroencephalography or electromyography. Signals can be recorded from cerebral
cortex, brain stem, spinal cord and peripheral nerves. Usually the term "evoked potential" is
reserved for responses involving either recording from, or stimulation of, central nervous
system structures. Sensory evoked potentials are recorded from the central nervous
system following stimulation of sense organs or by tactile or somatosensory evoked potential
elicited by tactile or electrical stimulation of a sensory or mixed nerve in the periphery. There
are three kinds of evoked potentials in widespread clinical use: auditory evoked potentials,
usually recorded from the scalp but originating at brainstem level; visual evoked potentials,
and somatosensory evoked potentials, which are elicited by electrical stimulation of peripheral
nerve. Motor evoked potentials are recorded from muscles following direct stimulation of
exposed motor cortex, or transcranial stimulation of motor cortex.
29) Electromyography.
Electromyography is a technique for evaluating and recording the electrical activity produced
by skeletal muscles. An electromyograph detects the electrical potential generated by
muscle cells when these cells are electrically or neurologically activated. The signals can be
analyzed to detect medical abnormalities. Muscle tissue at rest is normally electrically inactive.
After the electrical activity caused by the irritation of needle insertion subsides, the
electromyograph should detect no abnormal spontaneous activity. When the muscle is
voluntarily contracted, action potentials begin to appear. As the strength of the muscle
contraction is increased, more and more muscle fibers produce action potentials. When the
muscle is fully contracted, there should appear a disorderly group of action potentials of
varying rates and amplitudes. EMG is used to diagnose diseases that generally may be classified
into one of the following categories: neuropathies, neuromuscular junction
diseases and myopathies.
30) Neurosonography.
Neurosonography is an ultrasound-based diagnostic imaging technique used for visualizing
subcutaneous body structures including tendons, muscles, joints, vessels and internal organs
for possible lesions. It is possible to perform both diagnosis and therapeutic procedures, using

ultrasound to guide interventional procedures. Ultrasound information can be displayed in

several ways. A-mode: this display mode is the simplest; signals are recorded as spikes on a
graph. This type of ultrasonography is used for ophthalmologic scanning. B-mode (grayscale): this mode is most often used in diagnostic imaging. B-mode is commonly used to
evaluate the developing fetus and to evaluate organs. M-mode: this mode is used to image
moving structures. M-mode is used primarily for assessment of fetal heartbeat and in cardiac
imaging, most notably to evaluate valvular disorders. Doppler: this type of ultrasonography is
used to assess blood flow. Doppler ultrasonography uses the Doppler effect. The moving
objects are RBCs in blood.
31) Neuroroimaging.
Neuroimaging includes the use of various techniques to either directly or indirectly image the
structure, function/pharmacology of the brain. Neuroimaging falls into two broad categories:

Structural imaging, which deals with the structure of the brain and the diagnosis of gross
(large scale) intracranial disease (such as tumor), and injury, and

Functional imaging, which is used to diagnose metabolic diseases and lesions on a finer
scale (such as Alzheimer's disease) and also for neurological and cognitive
psychology research and building brain-computer interfaces.

Functional imaging enables the processing of information by centers in the brain to be

visualized directly. Such processing causes the involved area of the brain to increase
metabolism and "light up" on the scan. One of the more controversial uses of neuroimaging has
been research into mind-reading.
Computed axial tomography (CT scan): uses a series of x-rays of the head taken from many different
directions. Typically used for quickly viewing brain injuries. It uses a computer program that performs a
numerical integral calculation on the measured x-ray series to estimate how much of an x-ray beam is
absorbed in a small volume of the brain.

Magnetic resonance imaging (MRI): uses magnetic fields and radio waves to produce high
quality two-or three-dimensional images of brain structures without use of ionizing radiation
(X-rays) or radioactive tracers.
Functional magnetic resonance imaging (fMRI): slice at the level of the basal ganglia, showing
fMRI BOLD signal changes overlayed in red (increase) and blue (decrease) tones. It relies on the
paramagnetic properties of oxygenated and deoxygenated hemoglobin to see images of
changing blood flow in the brain associated with neural activity. This allows images to be
generated that reflect which brain structures are activated (and how) during performance of
different tasks. Most fMRI scanners allow subjects to be presented with different visual images,

sounds and touch stimuli, and to make different actions such as pressing a button or moving a
joystick.
32) Topical cortical syndromes.
Topical Cortical Syndromes:
FRONTAL LOBE SYNDROME
-Premotor area lesions: Adversive movements of the head and eyes, Conjugate paralysis of the
gaze, Grasp reflex, Cortical motor aphasia.
-Prefrontal area lesions: Disorders of executive function and impairment of the temporal
organization of movements: absence of active attention, reduced initiative of speech, Reduced
initiative (apathy, abulia), Disinhibition of behavior, Disturbances of micturition and defecation,
Contralateral ataxia, Ipsilateral anosmia.
PARIETAL LOBE SYNDROME
-Lesions of the postcentral gyrus: Jacksonian sensory epilepsy, Sensory deficit.
-Lesions of the anterior part of the superior parietal lobule: Loss of the sense of position and
passive movement, Loss of ability to distinguish objects by their size, shape, texture.
-Posterior parietal lesion syndrome: Disturbed perception of space (spatial agnosia) : left-right
spatial desorientation, constructional apraxia, neglect of one side of the body, anosognosia,
ideomotor apraxia, Disturbed assessment of the body schema (asomatognosia): autotpagnosia,
fingers agnosia, lefr-right body desorientation, Gerstmann`s syndrome.
TEMPORAL LOBE SYNDROME
-Irritative symptoms (temporal lobe epilepsy): Hallucinations with epigastric and abdominal
sensations, Automatisms (psychomotor acts or seizures).
-Negative symptoms: Cortical deafness, Auditory agnosia, Visual field defects, Sensory cortical
or Wernicke`s aphasia.
OCCIPITAL LOBE SYNDROME
-Irritative symptoms: Visual hallucinations.
-Visual deficits: Homonymous hemianopia, Quadrantanopia.
-Visual agnosias: simultanagnosia, prosopagnosia, Dyslexia without agraphia.

SYNDROME OF INTERNAL CAPSULE

Contralateral hemiparesis with central paresis of VIIth and XIIth cranial nerves
Contralateral hemihypoesthesia
Contralateral hemiataxia
Contralateral hemianopia

SYNDROMES OF SPINAL CORD LESIONS

Syndrome of spinal ganglion: herpes zoster: pain, reddening and vesicles in the
corresponding dermatome.
Syndrome of posterior root: anesthesia in complete damage or hypoalgesia,
paresthesias in incomplete damage in the corresponding dermatomes.
Syndrome of posterior tracts: loss of sensation for position and vibration in tabes
dorsalis ect.
Syndrome of posterior horn: dissociated sensory loss: loss of pain and temperature
sensation with preserved proprioreceptive sensation.
Syndrome of the gray matter: bilateral dissociated sensory loss: loss of pain and
temperature sensation in arms and chest.
Syndrome of combined damage of posterior funiculi and corticospinal tract: loss of
sensation for position and vibration + spastic paraparesis of the legs.
Syndrome of anterior horn: flaccid paralysis of the corresponding muscles with
fasciculations.
Syndrome of combined anterior horns and pyramidal tract damage in ALS: flaccid
paralysis + spastic paralysis.
Syndrome of corticospinal tract damage: progressive spinal spastic paralysis.
Syndrome of combined posterior funiculi, spinocerebellar tract and possibly
pyramidal tract damage: spinocerebellar and spinal ataxia, spastic paralysis in
Friedreich`s ataxia.
Syndrome of hemisection of the the spinal cord (Brown Sequard syndrome):
homolateral spastic paralysis and loss of position sense + contralateral loss of pain and
temperature sensation.
Syndrome of complete transection of the spinal cord: sudden: spinal shock (complete
tranverse flaccid paralysis + loss of all sensory modalities, abolished voluntary control of
bladder and rectum, trophic disorders of the skin below the lesion), slow developing:
spastic paralysis, abolished voluntary control of bladder and rectum, impotence,
autonomic abnormalities.
Syndromes of lesions at different levels of the spinal cord:

Above 5th cervical segment: quadriplegia and anesthesia of all sensory modalities
below the level of the lesion; retention of urine and feces; in bilateral lesion:
diaphragm paralysis
C5-C8 lesion: quadriplegia (flaccid in upper limbs, spastic in lower limbs); anesthesia
of all sensory modalities below the level of the lesion; retention of urine and feces
Th1-Th6 lesion: spastic paralysis in lower limbs; sensory loss below the level of the
lesion; possible difficulties in respiration and paralytic ileus
Th7 Th12 lesion: spastic paralysis in lower limbs; retention of urine and feces
L1-S2 lesion: lower flaccid paraplegia, anesthesia of all sensory modalities in
corresponding dermatomes in lower limbs, reflex empty of urine and feces
Syndrome of the conus (S3-S5): flaccid paralysis of the bladder with incontinence,
incontinence of feces, impotence, anesthesia of the perineum, absence of anal
reflex.
Syndrome of the cauda equina (L4-5, S1-5): radicular pain in the dermatomes of
affected roots, sensory disorders of all modalities in the dermatomes of affected
roots, + flaccid paralysis of the lower limbs, bladder and rectum.

BRAIN STEM SYNDROMES

MEDULLA OBLONGATA LESIONS:
UNILATERAL - Degerine`s syndrome - on the lesion side: flaccid paralysis with atrophy of
half of the tongue (n.XII), on the opposite side: spastic paralysis of arm and leg
(pyramidal tract). Wallenberg`s syndrome - on the lesion side: numbness and impaired
sensation for pain and temperature; ataxia of the limbs; vertigo, nystagmus; dysphagia,
dysphonia, diminishe or absent pharyngeal reflex, on the opposite side: impaired pain
and thermal sense over half of the body.
BILATERAL

SYNDOME OF PSEUDOBULBAR PALSY - dysarthria and dysphagia

SYNDROME OF BULBAR PALSY - dysarthria and dysphagia, flaccid paralysis of the

tongue

PONS LESIONS:
UNILATERAL - Millard-Gubler or Foville`s - on the lesion side: Peripheral facial paralysis;
diplopia on lateral gaze or conjugate horizontal gaze paralysis to the side of the lesion,
on the opposite side: hemiplegia or hemiparesis; impaired tactile and proprioceptive
sense over half of the body

MIDBRAIN LESIONS:
BILATERAL - Parinaud`s or Sylvian aqueduct syndrome: paralysis of conjugate upward
movement of gaze in the absence of paralysis of convergence. Argyll-Robertson`s
syndrome - small, irregular and unequal pupils, which do not dilate properly in response
to mydriatic drugs and fail to react to light, although they do constrict on
accommodation.
33) Syndromes of the internal capsule and the thalamus.
The internal capsule is an area of white matter in the brain that separates the caudate nucleus
and the thalamus from the putamen and the globus pallidus. The internal capsule contains both
ascending and descending axons. It consists of axonal fibres that run between the cerebral
cortex and the pyramids of the medulla.The internal capsule is V-shaped.
Pathology: The lenticulostriate arteries supply a substantial amount of the internal capsule.
These small vessels are particularly vulnerable to narrowing in the setting of chronic
hypertension and can result in small, punctate infarctions or intraparenchymal haemorrhage
due to vessel rupture. Lesions of the genu of the internal capsule affect fibers of the
corticobulbar tract. The primary motor cortex sends its axons through the posterior limb of the
internal capsule. Lesions, therefore, result in a contralateral hemiparesis or hemiplegia. While
symptoms of weakness due to an isolated lesion of the posterior limb can initially be severe,
recovery of motor function is sometimes possible due to spinal projections of premotor cortical
regions that are contained more rostrally in the internal capsule.
The thalamus is a midline symmetrical structure of two halves, within the brains , situated
between the cerebral cortex and the midbrain. Some of its functions are the relaying of sensory
and motor signals to the cerebral cortex, and the regulation of consciousness, sleep, and
alertness. The thalamus surrounds the third ventricle. It is the main product of the embryonic
diencephalon. A cerebrovascular accident (stroke) can lead to the thalamic syndrome, which
involves a one-sided burning or aching sensation often accompanied by mood swings. Bilateral
ischemia of the area supplied by the paramedian artery can cause serious problems including
akinetic mutism, and be accompanied by oculomotor problems. A related concept is
thalamocortical dysrhythmia. The occlusion of the artery of Percheron can lead to a bilateral
thalamus infarction.
Korsakoff's syndrome stems from damage to the mammillary body, the mammillothalamic
fasciculus or the thalamus.
Fatal familial insomnia is a hereditary prion disease in which degeneration of the thalamus
occurs, causing the patient to gradually lose his ability to sleep and progressing to a state of
total insomnia, which invariably leads to death.
34) Syndromes of the brainstem.

1. Webers syndrome: CN 3 palsy (pupil sparing) + contralateral hemiparesis.

2. Benedikts syndrome: Webers plus red nucleus - CN 3 palsy + contralateral hemiparesis +
contralateral hyperkinesis, ataxia, intention tremor: Weber + red nucleus.

3. Millard Gubler: CN 6 + CN 7 + contralateral hemiplegia.

4. Wallenbergs syndrome: dysphagia, ipsilateral vocal cord paralysis, vertigo, facial analgesia,
ipsilateral loss of taste.

5. Avellis syndrome: (tegmentum of the medulla) paralysis of soft palate and vocal cord +
contralateral hemianesthesia.

6. Jackson syndrome: ipsilateral tongue paralysis.

7. Medial medullary syndrome: (occlusion of basilar paramedian branches) ipsilateral
hemiparalysis of tongue + contralateral arm and leg hemiparesis.

8. Claude syndrome: (brachium conjunctivum) cerebellar ataxia + crossed CN III palsy.

9. Dysarthria-clumsy hand syndrome facial weakness and severe dysarthria and dysphagia that
occur in conjunction with a clumsy or paretic hand.

10. Nothnagel syndrome: unilateral or bilateral CN III + cerebellar ataxia.

11. Parinauds syndrome: loss of upward gaze + mydriasis (dilated pupil) + loss of convergence +
loss of pupillary light reflex + lid retraction + nystagmus retractorius.

12. Brain stem syndromes of non-vascular type: Foster-Kennedy lesions at the base of the frontal
lobe with symptoms of ipsilateral optic atrophy, ipsilateral anosmia, and contralateral
papilledema, Devics syndrome optic neuritis and myelitis and Lebers optic atrophy caused
by mitochondrial DNA mutation and usually causes a centrocecal scotoma.

35) Spinal cord syndromes.

SYNDROMES OF SPINAL CORD LESIONS
Syndrome of spinal ganglion: herpes zoster: pain, reddening and vesicles in the
corresponding dermatome.
Syndrome of posterior root: anesthesia in complete damage or hypoalgesia,
paresthesias in incomplete damage in the corresponding dermatomes.
Syndrome of posterior tracts: loss of sensation for position and vibration in tabes
dorsalis ect.
Syndrome of posterior horn: dissociated sensory loss: loss of pain and temperature
sensation with preserved proprioreceptive sensation.
Syndrome of the gray matter: bilateral dissociated sensory loss: loss of pain and
temperature sensation in arms and chest.

 Syndrome of combined damage of posterior funiculi and corticospinal tract: loss of

sensation for position and vibration + spastic paraparesis of the legs.
Syndrome of anterior horn: flaccid paralysis of the corresponding muscles with
fasciculations.
Syndrome of combined anterior horns and pyramidal tract damage in ALS: flaccid
paralysis + spastic paralysis.
Syndrome of corticospinal tract damage: progressive spinal spastic paralysis.
Syndrome of combined posterior funiculi, spinocerebellar tract and possibly
pyramidal tract damage: spinocerebellar and spinal ataxia, spastic paralysis in
Friedreich`s ataxia.
Syndrome of hemisection of the the spinal cord (Brown Sequard syndrome):
homolateral spastic paralysis and loss of position sense + contralateral loss of pain and
temperature sensation.
Syndrome of complete transection of the spinal cord: sudden: spinal shock (complete
tranverse flaccid paralysis + loss of all sensory modalities, abolished voluntary control of
bladder and rectum, trophic disorders of the skin below the lesion), slow developing:
spastic paralysis, abolished voluntary control of bladder and rectum, impotence,
autonomic abnormalities.
Syndromes of lesions at different levels of the spinal cord:
Above 5th cervical segment: quadriplegia and anesthesia of all sensory modalities
below the level of the lesion; retention of urine and feces; in bilateral lesion:
diaphragm paralysis
C5-C8 lesion: quadriplegia (flaccid in upper limbs, spastic in lower limbs); anesthesia
of all sensory modalities below the level of the lesion; retention of urine and feces
Th1-Th6 lesion: spastic paralysis in lower limbs; sensory loss below the level of the
lesion; possible difficulties in respiration and paralytic ileus
Th7 Th12 lesion: spastic paralysis in lower limbs; retention of urine and feces
L1-S2 lesion: lower flaccid paraplegia, anesthesia of all sensory modalities in
corresponding dermatomes in lower limbs, reflex empty of urine and feces
Syndrome of the conus (S3-S5): flaccid paralysis of the bladder with incontinence,
incontinence of feces, impotence, anesthesia of the perineum, absence of anal
reflex.
Syndrome of the cauda equina (L4-5, S1-5): radicular pain in the dermatomes of
affected roots, sensory disorders of all modalities in the dermatomes of affected
roots, + flaccid paralysis of the lower limbs, bladder and rectum.
36) Syndromes of the peripheral nervous system.

Peripheral neuropathy is the term for damage to nerves of the peripheral nervous system,
which may be caused either by diseases of or trauma to the nerve or the side-effects of
systemic illness. The four patterns of peripheral neuropathy
are: polyneuropathy, mononeuropathy, mononeuritis multiplex and autonomic neuropathy.
The most common form is (symmetrical) peripheral polyneuropathy, which mainly affects
the feet and legs. The form of neuropathy may be further broken down by cause, or the size of
predominant fiber involvement. Frequently the cause of a neuropathy cannot be identified and
it is designated idiopathic.
Mononeuropathy is a type of neuropathy that only affects a single nerve. The most common
cause of mononeuropathy is by physical compression of the nerve, known as compression
neuropathy. Carpal tunnel syndrome is one example of this. The "pins-and-needles" sensation
of one's "foot falling asleep" (paresthesia) is caused by a compression mononeuropathy. Direct
injury to a nerve, interruption of its blood supply (ischemia), or inflammation can also cause
mononeuropathy.
Mononeuritis multiplex is simultaneous involvement of individual noncontiguous nerve
trunks, either partially or completely, evolving over days to years and typically presents with
acute or subacute loss of sensory and motor function of individual peripheral nerves. The
pattern of involvement is asymmetric and as the disease progresses, becomes more
symmetrical, making it difficult to differentiate from polyneuropathy. Mononeuritis multiplex
may also cause pain, which is characterized as deep, aching pain that is worse at night, is
frequently in the lower back, hip, or leg.
Polyneuropathy many nerve cells in different parts of the body are affected, without regard
to thenerve through which they pass. Not all nerve cells are affected in any particular case. In
distal axonopathy, one common pattern, the cell bodies of neurons remain intact, but
the axons are affected in proportion to their length. Diabetic neuropathy is the most common
cause of this pattern. In demyelinating polyneuropathies, the myelin sheath around axons is
damaged, which affects the ability of the axons to conduct electrical impulses. The third and
least common pattern affects the cell bodies of neurones directly. This usually picks out either
the motor neurones (known as motor neurone disease) or the sensory neurones (known
as sensory neuronopathy).The effect of this is to cause symptoms in more than one part of the
body, often on left and right sides symmetrically.
Autonomic neuropathy is a form of polyneuropathy which affects the non-voluntary, nonsensory nervous system (ex. the autonomic nervous system) affecting mostly the internal
organs such as the bladder muscles, the cardiovascular system, the digestive tract, and
thegenital organs. These nerves are not under a person's conscious control and function
automatically. Autonomic nerve fibers form large collections in the thorax, abdomen and pelvis

outside spinal cord, however they have connections with the spinal cord and ultimately the
brain. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes
mellitus type 1 and 2. In most but not all cases, autonomic neuropathy occurs alongside other
forms of neuropathy, such as sensory neuropathy.
37) Meningeal syndrome. Syndrome of increased intracranial pressure. Idiopathic intracranial
hypertension.
Meningeal syndrome: is due to irritation of meninges of the brain and spinal cord. It arises
most often from inflammation of meninges but may occur in non-inflammatory diseases
subarachnoid hemorrhage, meningeal carcinomatosis, in which the carcinomatous cells spread
into the subarachnoid space. Signs: headache, bradycardia, nausea and vomiting, cervical
rigidity (stiffness of neck), Kernings sign positive (flexing the upper leg at a hip to a 90-degree
angle and then attempting to extend the knee). Meningism: there are symptoms of meningeal
irritation but in which no actual inflammation of meninges is present.
Some types:

Bacterial meningitis

Tuberculous meningitis

Viral meningitis

Increased intracranial pressure: increased intracranial pressure is a rise in the pressure inside
the skull that can result from or cause brain injury. Increased intracranial pressure can be due
to a rise in cerebrospinal fluid pressure. It can also be due to increased pressure within the
brain matter caused by a mass (such as a tumor), bleeding into the brain or fluid around the
brain, or swelling within the brain matter itself. The pressure itself can damage the brain or
spinal cord by pressing on important brain structures and by restricting blood flow into the
brain. Symptoms: vomiting, behavior changes, decreased consciousness, headache, seizures.
Idiopathic intracranial hypertension: characterized by increased intracranial pressure (pressure
around the brain) in the absence of a tumor or other diseases. The main symptoms are
headache, nausea, and vomiting, as well as pulsatile tinnitus (sounds perceived in the ears, with
the sound occurring in the same rhythm as the pulse), double vision and other visual
symptoms. If untreated, it may lead to swelling of the optic disc in the eye, which can progress
to vision loss. IIH is diagnosed with a brain scan and a lumbar puncture; lumbar puncture may
also provide temporary and sometimes permanent relief from the symptoms. The condition
may occur in all age groups, but is most common in young women, especially those with
obesity.