Chapter 5. Motor Deficits Part 4 (Tumors And Cord Compression)

Front 1

is a conspicuous feature—and usually the initial abnormality—in many patients with extradural lesions

Back 1

Pain

Front 2

is a conspicuous feature—and usually the initial abnormality—in many patients with extradural lesions

Back 2

Pain

Front 3

is a conspicuous feature—and usually the initial abnormality—in many patients with extradural lesions

Back 3

Pain

Front 4

Anterior Horn Cell Disorders

Back 4

wasting and weakness of the affected muscles without accompanying sensory changes. Electromyography shows changes that are characteristic of chronic partial denervation, with abnormal spontaneous activity in resting muscle and a reduction in the number of motor units under voluntary control; signs of reinnervation may also be present. Motor conduction velocity is usually normal but may be slightly reduced, and sensory conduction studies are normal. Muscle biopsy shows the histologic changes of denervation. Serum CK may be mildly elevated, but it never reaches the extremely high values seen in some muscular dystrophies

Front 5

Anterior Horn Cell Disorders

Back 5

wasting and weakness of the affected muscles without accompanying sensory changes. Electromyography shows changes that are characteristic of chronic partial denervation, with abnormal spontaneous activity in resting muscle and a reduction in the number of motor units under voluntary control; signs of reinnervation may also be present. Motor conduction velocity is usually normal but may be slightly reduced, and sensory conduction studies are normal. Muscle biopsy shows the histologic changes of denervation. Serum CK may be mildly elevated, but it never reaches the extremely high values seen in some muscular dystrophies

Front 6

Anterior Horn Cell Disorders

Back 6

wasting and weakness of the affected muscles without accompanying sensory changes. Electromyography shows changes that are characteristic of chronic partial denervation, with abnormal spontaneous activity in resting muscle and a reduction in the number of motor units under voluntary control; signs of reinnervation may also be present. Motor conduction velocity is usually normal but may be slightly reduced, and sensory conduction studies are normal. Muscle biopsy shows the histologic changes of denervation. Serum CK may be mildly elevated, but it never reaches the extremely high values seen in some muscular dystrophies

Front 7

Anterior Horn Cell Disorders

Back 7

wasting and weakness of the affected muscles without accompanying sensory changes. Electromyography shows changes that are characteristic of chronic partial denervation, with abnormal spontaneous activity in resting muscle and a reduction in the number of motor units under voluntary control; signs of reinnervation may also be present. Motor conduction velocity is usually normal but may be slightly reduced, and sensory conduction studies are normal. Muscle biopsy shows the histologic changes of denervation. Serum CK may be mildly elevated, but it never reaches the extremely high values seen in some muscular dystrophies

Front 8

Anterior Horn Cell Disorders

Back 8

wasting and weakness of the affected muscles without accompanying sensory changes. Electromyography shows changes that are characteristic of chronic partial denervation, with abnormal spontaneous activity in resting muscle and a reduction in the number of motor units under voluntary control; signs of reinnervation may also be present. Motor conduction velocity is usually normal but may be slightly reduced, and sensory conduction studies are normal. Muscle biopsy shows the histologic changes of denervation. Serum CK may be mildly elevated, but it never reaches the extremely high values seen in some muscular dystrophies

Front 9

Werdnig-Hoffmann Disease or

Back 9

SMA-I)

This autosomal recessive disorder usually manifests itself within the first 3 months of life. The infant is floppy and may have difficulty with sucking, swallowing, or ventilation. In established cases, examination reveals impaired swallowing or sucking, atrophy and fasciculation of the tongue, and muscle wasting in the limbs that is sometimes obscured by subcutaneous fat. The tendon reflexes are normal or depressed, and the plantar responses may be absent. There is no sensory deficit. The disorder is rapidly progressive, generally leading to death from respiratory complications by approximately age 3.

Front 10

Werdnig-Hoffmann Disease or

Back 10

SMA-I)

This autosomal recessive disorder usually manifests itself within the first 3 months of life. The infant is floppy and may have difficulty with sucking, swallowing, or ventilation. In established cases, examination reveals impaired swallowing or sucking, atrophy and fasciculation of the tongue, and muscle wasting in the limbs that is sometimes obscured by subcutaneous fat. The tendon reflexes are normal or depressed, and the plantar responses may be absent. There is no sensory deficit. The disorder is rapidly progressive, generally leading to death from respiratory complications by approximately age 3.

Front 11

Werdnig-Hoffmann Disease or

Back 11

SMA-I)

This autosomal recessive disorder usually manifests itself within the first 3 months of life. The infant is floppy and may have difficulty with sucking, swallowing, or ventilation. In established cases, examination reveals impaired swallowing or sucking, atrophy and fasciculation of the tongue, and muscle wasting in the limbs that is sometimes obscured by subcutaneous fat. The tendon reflexes are normal or depressed, and the plantar responses may be absent. There is no sensory deficit. The disorder is rapidly progressive, generally leading to death from respiratory complications by approximately age 3.

Front 12

Werdnig-Hoffmann Disease or

Back 12

SMA-I)

This autosomal recessive disorder usually manifests itself within the first 3 months of life. The infant is floppy and may have difficulty with sucking, swallowing, or ventilation. In established cases, examination reveals impaired swallowing or sucking, atrophy and fasciculation of the tongue, and muscle wasting in the limbs that is sometimes obscured by subcutaneous fat. The tendon reflexes are normal or depressed, and the plantar responses may be absent. There is no sensory deficit. The disorder is rapidly progressive, generally leading to death from respiratory complications by approximately age 3.

Front 13

This autosomal recessive disorder usually manifests itself within the first 3 months of life. The infant is floppy and may have difficulty with sucking, swallowing, or ventilation. In established cases, examination reveals impaired swallowing or sucking, atrophy and fasciculation of the tongue, and muscle wasting in the limbs that is sometimes obscured by subcutaneous fat. The tendon reflexes are normal or depressed, and the plantar responses may be absent. There is no sensory deficit. The disorder is rapidly progressive, generally leading to death from respiratory complications by approximately age 3.

Back 13

SMA-I/wernigg -hoffman

Front 14

This autosomal recessive disorder usually manifests itself within the first 3 months of life. The infant is floppy and may have difficulty with sucking, swallowing, or ventilation. In established cases, examination reveals impaired swallowing or sucking, atrophy and fasciculation of the tongue, and muscle wasting in the limbs that is sometimes obscured by subcutaneous fat. The tendon reflexes are normal or depressed, and the plantar responses may be absent. There is no sensory deficit. The disorder is rapidly progressive, generally leading to death from respiratory complications by approximately age 3.

Back 14

SMA-I/wernigg -hoffman

Front 15

This autosomal recessive disorder usually manifests itself within the first 3 months of life. The infant is floppy and may have difficulty with sucking, swallowing, or ventilation. In established cases, examination reveals impaired swallowing or sucking, atrophy and fasciculation of the tongue, and muscle wasting in the limbs that is sometimes obscured by subcutaneous fat. The tendon reflexes are normal or depressed, and the plantar responses may be absent. There is no sensory deficit. The disorder is rapidly progressive, generally leading to death from respiratory complications by approximately age 3.

Back 15

SMA-I/wernigg -hoffman

Front 16

may reduce mortality and slow progression of amyotrophic lateral sclerosis, possibly because it blocks glutamatergic transmission in the CNS.

Back 16

Riluzole (100 mg daily)

Front 17

may reduce mortality and slow progression of amyotrophic lateral sclerosis, possibly because it blocks glutamatergic transmission in the CNS.

Back 17

Riluzole (100 mg daily)

Front 18

may reduce mortality and slow progression of amyotrophic lateral sclerosis, possibly because it blocks glutamatergic transmission in the CNS.

Back 18

Riluzole (100 mg daily)

Front 19

may reduce mortality and slow progression of amyotrophic lateral sclerosis, possibly because it blocks glutamatergic transmission in the CNS.

Back 19

Riluzole (100 mg daily)

Front 20

Its clinical characteristics include tremor (resembling essential tremor), cramps, fasciculations, proximal weakness, and twitching movements of the chin that are precipitated by pursing of the lips.

Back 20

Bulbospinal neuronopathy (Kennedy syndrome) is a sex-linked recessive disorder associated with an expanded trinucleotide repeat sequence on the androgen receptor gene. It has a more benign prognosis than the other motor neuron diseases.

Front 21

Its clinical characteristics include tremor (resembling essential tremor), cramps, fasciculations, proximal weakness, and twitching movements of the chin that are precipitated by pursing of the lips.

Back 21

Bulbospinal neuronopathy (Kennedy syndrome) is a sex-linked recessive disorder associated with an expanded trinucleotide repeat sequence on the androgen receptor gene. It has a more benign prognosis than the other motor neuron diseases.

Front 22

Its clinical characteristics include tremor (resembling essential tremor), cramps, fasciculations, proximal weakness, and twitching movements of the chin that are precipitated by pursing of the lips.

Back 22

Bulbospinal neuronopathy (Kennedy syndrome) is a sex-linked recessive disorder associated with an expanded trinucleotide repeat sequence on the androgen receptor gene. It has a more benign prognosis than the other motor neuron diseases.

Front 23

Its clinical characteristics include tremor (resembling essential tremor), cramps, fasciculations, proximal weakness, and twitching movements of the chin that are precipitated by pursing of the lips.

Back 23

Bulbospinal neuronopathy (Kennedy syndrome) is a sex-linked recessive disorder associated with an expanded trinucleotide repeat sequence on the androgen receptor gene. It has a more benign prognosis than the other motor neuron diseases.

Front 24

Its clinical characteristics include tremor (resembling essential tremor), cramps, fasciculations, proximal weakness, and twitching movements of the chin that are precipitated by pursing of the lips.

Back 24

Bulbospinal neuronopathy (Kennedy syndrome) is a sex-linked recessive disorder associated with an expanded trinucleotide repeat sequence on the androgen receptor gene. It has a more benign prognosis than the other motor neuron diseases.

Front 25

Acute paralytic poliomyelitis is another manifestation and is characterized by acute, focal or generalized, asymmetric weakness or by a rapidly ascending quadriplegia that may be mistaken for the Guillain-Barre syndrome.

Back 25

West Nile Virus Infection

West Nile virus infection is acquired from infected mosquitos. Its most common manifestation is meningoencephalitis.

Front 26

Acute paralytic poliomyelitis is another manifestation and is characterized by acute, focal or generalized, asymmetric weakness or by a rapidly ascending quadriplegia that may be mistaken for the Guillain-Barre syndrome.

Back 26

West Nile Virus Infection

West Nile virus infection is acquired from infected mosquitos. Its most common manifestation is meningoencephalitis.

Front 27

Acute paralytic poliomyelitis is another manifestation and is characterized by acute, focal or generalized, asymmetric weakness or by a rapidly ascending quadriplegia that may be mistaken for the Guillain-Barre syndrome.

Back 27

West Nile Virus Infection

West Nile virus infection is acquired from infected mosquitos. Its most common manifestation is meningoencephalitis.

Front 28

Acute paralytic poliomyelitis is another manifestation and is characterized by acute, focal or generalized, asymmetric weakness or by a rapidly ascending quadriplegia that may be mistaken for the Guillain-Barre syndrome.

Back 28

West Nile Virus Infection

West Nile virus infection is acquired from infected mosquitos. Its most common manifestation is meningoencephalitis.

Front 29

Acute paralytic poliomyelitis is another manifestation and is characterized by acute, focal or generalized, asymmetric weakness or by a rapidly ascending quadriplegia that may be mistaken for the Guillain-Barre syndrome.

Back 29

West Nile Virus Infection

West Nile virus infection is acquired from infected mosquitos. Its most common manifestation is meningoencephalitis.

Front 30

An L5 radiculopathy causes

Back 30

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 31

An L5 radiculopathy causes

Back 31

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 32

An L5 radiculopathy causes

Back 32

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 33

An L5 radiculopathy causes

Back 33

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 34

An L5 radiculopathy causes

Back 34

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 35

An L5 radiculopathy causes

Back 35

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 36

An L5 radiculopathy causes

Back 36

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 37

An L5 radiculopathy causes

Back 37

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 38

An L5 radiculopathy causes

Back 38

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 39

An L5 radiculopathy causes

Back 39

weakness of dorsiflexion of the foot and toes, whereas S1 root involvement produces weakness of plantar flexion of the foot and a depressed ankle jerk

Front 40

weakness of plantar flexion of the foot and a depressed ankle jerk

Back 40

S1 root involvement

Front 41

weakness of plantar flexion of the foot and a depressed ankle jerk

Back 41

S1 root involvement

Front 42

weakness of plantar flexion of the foot and a depressed ankle jerk

Back 42

S1 root involvement

Front 43

weakness of plantar flexion of the foot and a depressed ankle jerk

Back 43

S1 root involvement

Front 44

weakness of plantar flexion of the foot and a depressed ankle jerk

Back 44

S1 root involvement

Front 45

Lasegue sign

Back 45

Straight-leg raising in the supine position is restricted, often to approximately 20 or 30 degrees of hip flexion, from a normal value of 80 or 90 degrees, because of reflex spasm of the hamstring muscles

Front 46

Lasegue sign

Back 46

Straight-leg raising in the supine position is restricted, often to approximately 20 or 30 degrees of hip flexion, from a normal value of 80 or 90 degrees, because of reflex spasm of the hamstring muscles

Front 47

Lasegue sign

Back 47

Straight-leg raising in the supine position is restricted, often to approximately 20 or 30 degrees of hip flexion, from a normal value of 80 or 90 degrees, because of reflex spasm of the hamstring muscles

Front 48

Lasegue sign

Back 48

Straight-leg raising in the supine position is restricted, often to approximately 20 or 30 degrees of hip flexion, from a normal value of 80 or 90 degrees, because of reflex spasm of the hamstring muscles

Front 49

Lasegue sign

Back 49

Straight-leg raising in the supine position is restricted, often to approximately 20 or 30 degrees of hip flexion, from a normal value of 80 or 90 degrees, because of reflex spasm of the hamstring muscles

Front 50

Straight-leg raising in the supine position is restricted, often to approximately 20 or 30 degrees of hip flexion, from a normal value of 80 or 90 degrees, because of reflex spasm of the hamstring muscles

Back 50

Lasegue sign)

Front 51

Straight-leg raising in the supine position is restricted, often to approximately 20 or 30 degrees of hip flexion, from a normal value of 80 or 90 degrees, because of reflex spasm of the hamstring muscles

Back 51

Lasegue sign)

Front 52

Erb-Duchenne Paralysis

Back 52

Traumatic avulsion of the C5 and C6 roots can occur at birth as a result of traction on the head during delivery of the shoulder. It can also be the result of injuries causing excessive separation of the head and shoulder. It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 53

Erb-Duchenne Paralysis

Back 53

Traumatic avulsion of the C5 and C6 roots can occur at birth as a result of traction on the head during delivery of the shoulder. It can also be the result of injuries causing excessive separation of the head and shoulder. It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 54

Erb-Duchenne Paralysis

Back 54

Traumatic avulsion of the C5 and C6 roots can occur at birth as a result of traction on the head during delivery of the shoulder. It can also be the result of injuries causing excessive separation of the head and shoulder. It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 55

Erb-Duchenne Paralysis

Back 55

Traumatic avulsion of the C5 and C6 roots can occur at birth as a result of traction on the head during delivery of the shoulder. It can also be the result of injuries causing excessive separation of the head and shoulder. It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 56

Erb-Duchenne Paralysis

Back 56

Traumatic avulsion of the C5 and C6 roots can occur at birth as a result of traction on the head during delivery of the shoulder. It can also be the result of injuries causing excessive separation of the head and shoulder. It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 57

Erb-Duchenne Paralysis (c5-c6) leads to?

Back 57

It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 58

Erb-Duchenne Paralysis (c5-c6) leads to?

Back 58

It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 59

Erb-Duchenne Paralysis (c5-c6) leads to?

Back 59

It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 60

Erb-Duchenne Paralysis (c5-c6) leads to?

Back 60

It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 61

Erb-Duchenne Paralysis (c5-c6) leads to?

Back 61

It leads to loss of shoulder abduction and elbow flexion. In consequence, the affected arm is held internally

Front 62

Klumpke Paralysis

Involvement of the what roots?

Back 62

C8 and T1 roots causes paralysis and wasting of the small muscles of the hand and of the long finger flexors and extensors. Horner syndrome is sometimes an associated finding. This kind of lower

Front 63

Klumpke Paralysis

Involvement of the what roots?

Back 63

C8 and T1 roots causes paralysis and wasting of the small muscles of the hand and of the long finger flexors and extensors. Horner syndrome is sometimes an associated finding. This kind of lower

Front 64

Klumpke Paralysis

Involvement of the what roots?

Back 64

C8 and T1 roots causes paralysis and wasting of the small muscles of the hand and of the long finger flexors and extensors. Horner syndrome is sometimes an associated finding. This kind of lower

Front 65

Klumpke Paralysis

Involvement of the what roots?

Back 65

C8 and T1 roots causes paralysis and wasting of the small muscles of the hand and of the long finger flexors and extensors. Horner syndrome is sometimes an associated finding. This kind of lower

Front 66

Klumpke Paralysis

Involvement of the what roots?

Back 66

C8 and T1 roots causes paralysis and wasting of the small muscles of the hand and of the long finger flexors and extensors. Horner syndrome is sometimes an associated finding. This kind of lower