13. Laboratory Screening for “Treatable”
Neuropathy?
B12
Diabetes This type of neuropathy
generally a late finding
ANA, chronic disease
screen
Screen for connective tissue
diseases (late finding)
TSH
ESR If onset is recent
HIV Risk Factors
Review medications
16. Mononeuropathy
• Focal lesion involving a single nerve
• Electro diagnostic studies indispensible
– Localize site of injury
– Determine severity of lesion
23. Polyneuropathy
• Evolution is centripetal
– Symptoms spread up legs
• Sensory loss
• Dysesthesias
– Ankles jerks are depressed
– Patients have trouble walking on their heels
– Foot plantar flexion remains strong
24. Polyneuropathy
–Symptoms noticed in fingertips
• Numbness
• Dysesthesias
• Advanced picture is easily recognizable
– Stocking-glove sensory loss
– Distal muscle wasting and weakness
– Absent tendon reflexes
25. Polyneuropathy
• Sub classification
– Historical features are indispensible
• Other medical conditions
• Symptoms of systemic disease
• Recent viral or other infectious diseases
• Recent vaccinations
• Institution of new medications
26. Polyneuropathy
• Exposure to toxins
– Alcohol
– Heavy metals
– Organic solvents
• Family history
• Duration and clinical course are helpful
– Acute = days to weeks
– Chronic = months to years
30. Treatment
–Preventative and palliative
• Weight reduction
• Assiduous foot care
• Good shoes
• Ankle-foot orthoses as needed
• Several organizations provide support
32. Definition
Parkinson disease (Parkinson's disease,
PD) is a progressive neurodegenerative
disorder associated with a loss of
dopaminergic nigrostriatal neurons.
It is named after James Parkinson, the
English physician who described the
shaking palsy in 1817
33. Parkinson disease is recognized as one of
the most common neurological disorders,
affecting approximately 1% of individuals
older than 60 years.
Cardinal features include resting tremor,
rigidity, bradykinesia (a paucity and slowness
of movement), and postural instability
34. Epidemiology
PD afflicts ~1 million individuals in the
United States (~1% of those over 55
years).
Its peak age of onset is in the early 60s
(range 35–85 years), and the course of the
illness ranges between 10 and 25 years.
PD accounts for ~75% of all cases of
parkinsonism; the remaining cases result
from other neurodegenerative disorders,
cerebrovascular disease, and drugs.
Familial forms of known autosomal
dominant and recessive forms of PD (now
35. These are generally characterized by an
earlier age of onset (typically before age
45 years) and a longer course than cases
of "sporadic" PD, although one genetic
form, LLRK-2, causes PD in the same age
range as sporadic PD.
Although most patients with PD appear to
have no strong genetic determinant,
epidemiologic evidence points to a
complex interaction between genetic
36. Risk factors include a positive family history, male
gender, head injury, exposure to pesticides.
Factors associated with a reduced incidence of PD
include coffee drinking, smoking, use of
nonsteroidal anti-inflammatory drugs, and
estrogen replacement in postmenopausal women
37. Pathophysiology
The major neuropathologic findings in
Parkinson disease are a loss of pigmented
dopaminergic neurons in the substantia
nigra and the presence of Lewy bodies.
The loss of dopaminergic neurons occurs
most prominently in the ventral lateral
substantia nigra.
Approximately 60-80% of dopaminergic
neurons are lost before the motor signs of
Parkinson disease emerge
38. Clinical Features
A diagnosis of PD can be made with some
confidence in patients who present with at
least two of the three cardinal signs—rest
tremor, rigidity, and bradykinesia.
Tremor is particularly important, as it is
present in 85% of patients with true PD; a
diagnosis of PD is particularly difficult
when tremor is absent.
39. A unilateral and gradual onset of
symptoms further supports the diagnosis.
Masked facies, decreased eye blinking,
stooped posture, and decreased arm
swing complete the early picture.
The onset may also be heralded by vague
feelings of weakness, fatigue, aching, and
discomfort
40. Motor Features
The most disabling motor feature of PD is
bradykinesia, which interferes with all
aspects of daily living including rising from
a chair, walking, turning in bed, and
dressing.
Fine motor control is also impaired, as
evidenced by decreased manual dexterity
and micrographia.
Soft speech (hypophonia) and sialorrhea
are other troubling manifestations of
(bulbar) bradykinesia.
Rest tremor, typically appears unilaterally,
41. Tremor usually spreads proximally and
occasionally to the ipsilateral leg before appearing
on the other side after a year or more.
It may appear later in the lips, tongue, and jaw but
spares the head and neck.
Rigidity is felt as a uniform resistance to passive
movement about a joint throughout the full range
of motion, accompanied by a characteristic
"plastic" quality to the movement.
Brief, regular interruptions of resistance during
passive movement, due to subclinical tremor, may
give rise to a "cogwheeling" sensation.
• Dystonia involving the distal arm or leg may occur
early in the disease, unrelated to treatment,
42. It can also be provoked by
antiparkinsonian drug therapy
Gait disturbance with shuffling short steps
and a tendency to turn en bloc is a
prominent feature of PD.
Festinating gait, a classic sign of
Parkinsonism, results from the
combination of flexed posture and loss of
postural reflexes, which cause the patient
to accelerate in an effort to "catch up" with
43. Freezing of gait, a feature of more advanced
PD, occurs commonly at the onset of
locomotion (start hesitation), when attempting
to change direction or turn around, and upon
entering a crowded room or narrow space
such as a doorway
Abnormalities of balance and posture tend to
increase as the disease progresses.
Flexion of the head, stooping and tilting of the
upper trunk, and a tendency to hold the arm
in a flexed posture while walking are
common, as are changes in the posture of
44. Non-Motor Features
Non-motor aspects of PD include depression
and anxiety, cognitive impairment, sleep
disturbances, sensory abnormalities and
pain, loss of smell (anosmia), and
disturbances of autonomic function
Sensory symptoms often manifest as a
distressing sensation of inner restlessness
presumed to be a form of akathisia
Sleep disorders and impaired daytime
alertness are common in PD
• Autonomic dysfunction can produce diverse
manifestations, including orthostatic
hypotension, constipation, urinary urgency
and frequency, excessive sweating, and
45. Neuropsychiatric Symptoms
Changes in mood, cognition, and behavior
are common accompaniments of PD,
especially in its later stages, and may be
the direct result of PD or its comorbid
pathologies [e.g., Alzheimer's disease
(AD), cortical dementia with Lewy bodies
(DLB)] or may occur as a side effect of
antiparkinsonian or concomitant therapy
Depression affects approximately half of
patients with PD and can occur at any
46. Treatment
The goals of therapy in PD are to maintain
function and quality of life and to avoid
drug-induced complications.
Bradykinesia, tremor, rigidity, and
abnormal posture respond well to
symptomatic therapy early in the course of
the illness.
In contrast, cognitive symptoms,
hypophonia, autonomic dysfunction, and
imbalance tend to respond poorly.
47. Initiation of Therapy
From a practical standpoint,
dopaminomimetic therapy should be
initiated as soon as the patient's
symptoms begin to interfere with quality of
life.
The ideal first-line agent depends on the
age and cognitive status of the patient
and, to a lesser extent, the patient's
clinical type and finances.
The choices consist of either a dopamine
Editor's Notes
Myelin : Current cannot flow
Axon : No nerves left
Innervation- skeletal muscle and autonomic system.
