Professional Documents
Culture Documents
TH Cliniclas of Neuroanatomy
TH Cliniclas of Neuroanatomy
Spinal Cord
Anterior Cord syndrome ( due to injury of anterior spinal artery or vertebral fracture)
Level of spinal cord lesion Clinical sign Cause
At the level of lesion Bilateral lower motor neuron Damage of anterior gray
paralysis & muscular atrophy column (LMN lesion)
Below the level of lesion Bilateral Upper motor neuron
lesion i.e;
Bilateral spastic paralysis Corticospinal & other
descending tracts
Bilateral loss of pain,
temperature, and light touch Damage to anterior & lateral
sensations. spinothalamic tracts
➢ Tactile discrimination and vibratory and proprioceptive sensations are preserved because
the posterior white columns on both sides are undamaged.
➢ Central cord syndrome is most often caused by hyperextension of the cervical region of
the spine. The cord is pressed on anteriorly by the vertebral bodies and posteriorly by
the bulging of the ligamentum flavum. There is
At the level of lesion; there is lower motor neuron lesion.
Below the level of lesion;
1)There is upper motor neuron lesion. The lower limb fibers are affected less than the upper
limb fibers because the descending fibers in the lateral corticospinal tracts are laminated,
with the upper limb fibers located medially and the lower limb fibers located laterally.
2)Bilateral loss of pain, temperature, light touch, and pressure sensations with
characteristic sacral sparing.Because the ascending fibers in the lateral and anterior
spinothalamic tracts are also laminated, with the upper limb fibers located medially and
the lower limb fibers located laterally, the upper limb fibers are more susceptible to
damage than the lower limb fibers.
Brainstem
Cerebellum
➢ Cerebellar disease: Lesion in one cerebellar hemisphere gives rise to signs and symptoms that
are limited to the same side of the body. It includes
1)Hypotonia (diminished muscle tone)
2)Postural Changes and Gait: Head is often rotated and flexed, and the shoulder on the side
ofthe lesion is lower than on the normal side. The patient assumes a widebase when he or she
stands and is often stiff legged to compensate forloss of muscle tone. When the individual
walks, he or she lurches and staggers toward the affected side.These are more pronounced
with the eyes closed (Romberg’s sign).
3)Ataxia (Disturbances of Voluntary Movement):The muscles contract irregularly and
weakly.Intention Tremors occurs when fine movement ( buttoning clothes,writing,and
shaving).
4)Asynergia: Muscle groups fail to work harmoniously,and there is decomposition of
movement.When patient is asked to touch tip of the nose with the index finger, movements
are not properly coordinated, and the finger either passes the nose (past-pointing) orhits the
nose.
5)Dysdiadochokinesia is the inability to perform alternating movementsregularly and rapidly.
Ask the patient to pronate and supinate theforearms rapidly.
6)Reflexes: Movement produced by tendon reflexes tends to continue for a longer period of
time than normal i.e;The pendular knee jerk
7)Nystagmus, which is ataxia of the ocular muscles, is arhythmical oscillation of the eyes. It is
more easily demonstrated whenthe eyes are deviated in a horizontal direction. This rhythmic
oscillationof the eyes may be of the same rate in both directions (pendular nystagmus) or
quicker in one direction than in the other (jerk nystagmus).
8)Dysarthria is ataxia of the muscles of the larynx.Articulation is jerky, and the syllables are
separated from one another.Speech tends to be explosive and syllables are slurred.
Cerebrum
➢ Thalamic syndrome occurs due to vascular lesionof thalamic branch of posterior cerebral
artery.1) Threshold for appreciation of touch,pain,temperature is lowered. 2)Sensation that is
normal may appear to be exaggerated or unpleasant. 3)There may be spontaneous pain.
4)Emotions may be abnormal.
Part of cerebrum affected Sign & symptom
Primary motor area (4) Contralateral monoplegia ( hemiplegia)
Jacksonian Epileptic seizures
Premotor area (6) Apraxia (Skilled movements are affected)
Frontal eye field (8) Deviation of eyes to side of lesion
Prefrontal area (9,10,11,12) Personality changes
Motor speech area / Broca(44,45) Expressive/motor aphasia–Difficulty in spoken
speech or writing (agraphia). Non-fluent speech
and telegraphic language. Key words spoken are
normal.
First somatosensory area (1,2,3) Contralateral sensory loss
Second somatosensory area inability to appreciate pain and temperature
areas behind the main sensory area (areas 5 Inability to identify objects by feeling them
and 7)
Sensory speech area/Wernicke area (40) Receptive/sensory aphasia–Loss of ability to
understand spoken and written speech. Spoken
speech is fluent but contains paraphasias
(substitution of a word with a non-word, out of
context word, and neologism)
Left perisylvian area (Broca + wernicke area) Global aphasia (sensory & motor aphasia)
Primary auditory area (41, 42) Slight bilateral loss of hearing if one side is
affected. Bilateral involvement of auditory area
will result in deafness.
Auditory association area (22) Word deafness (auditory verbal agnosia)–
Inability to interpret meaning of the sounds
heard
Primary visual area (17) Contralateral homonymous hemianopia with
macular sparing in vascular lesions (No macular
sparing in trauma or tumours)
Visual association area (18, 19) Visual agnosia–Loss of ability to recognize
objects, Word blindness–alexia
Basal Ganglia
➢ Disorders of the basal nuclei are of two general types.Hyperkinetic disorders ( excessive &
abnormal movements) i.e; chorea, athetosis, and ballism. Hypokinetic disorders ( lack or
slowness of movement).Parkinson disease includes both types of motor disturbances.
➢ Chorea involves involuntary, quick, jerky, irregular movements that are nonrepetitive i.e; Swift
grimaces and sudden movements of the head or limbs
➢ Huntington disease is autosomal dominant disease.There is a single gene defect on
chromosome 4.This gene encodes a protein, huntingtin.The codon (CAG) that encodes
glutamine is repeated many more times than normal.There is degeneration of the GABA-
secreting & acetylcholine-secreting neurons of striatonigral-inhibiting pathway. This results in
the dopa-secreting neurons of the substantia nigra becoming overactive; thus, nigrostriatal
pathway inhibits the caudate nucleus and the putamen.Disease involves:
1. Choreiform movements ( involuntary movements of extremities) and twitching of the face
(facial grimacing). Later,more muscle groups are involved, so the patient becomes immobile
and unable to speak or swallow. 2. Progressive dementia occurs with loss of memory and
intellectual capacity.
➢ Sydenham chorea (St. Vitus' dance) is disease of childhood in which there are rapid, irregular,
involuntary movements of the limbs, face,and trunk.The condition is associated with
rheumatic fever. Antigens of the streptococcal bacteria are similar in structure to proteins
present in the membranes of striatal neurons.The host's antibodies not only combine with
bacterial antigens but also attack membranes of neurons of basal ganglia.
➢ Hemiballismus is a form of involuntary movement confined to one side of the body. It involves
the proximal extremity musculature,andthe limb suddenly flies about out of control in all
directions.The lesion (small stroke)occurs in the opposite subthalamic nucleus.
➢ Parkinson Disease: There is degeneration of the neurons of substantia nigra (that send their
axons to corpus striatum) & it results in reduction in the release of neurotransmitter
dopamine within corpus striatum.This leads to hypersensitivity of the dopamine receptors in
the postsynaptic neurons in the striatum.Following signs & symptoms ( PAR)
1)P= Postural disturbances: Patient stands with a stoop with arms flexed. The patient walks by
taking short steps and often is unable to stop.
2)A=Akinesia:There is a difficulty in initiating and performing new movements.The
movements are slow, the face is expressionless, and the voice is slurred and unmodulated.
Swinging of the arms in walking is lost.
3)R=Rigidity. This differs from the rigidity caused by lesions of the uppermotor neurons in that
it is present to an equal extent in opposing muscle groups.If tremor is absent, the rigidity is
felt as resistance to passive movement (plastic rigidity). If the tremor is present,muscle
resistance is overcome as a series of jerks, called (cogwheel rigidity).
4)R=Resting Tremor (due to alternating contraction of agonists & antagonists).
There is no loss of muscle power and no loss of sensibility. Since corticospinal tracts are
normal, the superficial abdominal reflexes are normal, and there is no Babinski response. The
deep tendon reflexes are normal.
Postencephalitic parkinsonism developed following the viral encephalitis outbreak of 1916-
17 .Iatrogenic parkinsonism can be a side effect of antipsychotic drugs (drugs which block D2
receptors)e.g., phenothiazines,Meperidine analogues.Atherosclerotic parkinsonism can occur
in elderly hypertensive patients. Treatment includes
1)By elevating brain dopamine level. Unfortunately, dopamine cannot cross the blood-brain
barrier, but its immediate precursor L-dopa can and is used.
2) Selegiline inhibits monoamine oxidase, which is responsible for destroying dopamine
3)Transplantation of human embryonic dopamine-producing neurons into the caudate
nucleus and putamen & Pallidotomy (surgical lesions in the globus pallidus).
➢ Athetosis consists of slow, sinuous, writhing movements that mostcommonly involve the
distal segments of the limbs. Degeneration of globus pallidus occurs with a breakdown of the
circuitry involving thebasal nuclei and the cerebral cortex.
Written by