1. Ericsson and Kintsch (1995) hypothesize that people store not only information but also learning strategies in long-term memory for easy access. This capacity, which Ericsson and Kintsch call long-term working memory, accounts for the extraordinary skills of experts (such as medical diagnosticians) who must match current information with a vast array of patterns held in their long-term memories.

A problem that occurs during or after a trip does not necessarily need to have a causal connection with that trip. Frequent causes of acute confusion are cerebral malaria, side effects of mefloquine, febrile delirium, acute meningitis. In acute confusion, delirium or psychosis you should:

• check the vital signs

• look for neck stiffness and consider LP

• determine whether the patient has a high temperature or not

• upon suspicion of hypoglycaemia, glucose should be administered immediately, preferably with thiamine

• perform full blood count and thick smear

Delirium can occur in many febrile diseases. Confusion is prominent in typhoid fever, rickettsiosis, cerebral malaria, viral encephalitis (rabies, herpes, Japanese encephalitis, West Nile and other arboviroses), Naegleria fowleri encephalitis (amoebae), acute meningitis and cerebral abscess (tuberculous, pyogenic or amoebiasis). Endocarditis can cause septic cerebral emboli. Cerebritis and cerebellitis with ataxia can occur in Q-fever and also very rarely in Mycoplasma infections.

Syphilitic cerebral gumma, West African trypanosomiasis and cerebral toxoplasmosis cause a subacute to chronic condition. Differentiation from dementia is important. Melarsoprol used in the treatment of African trypanosomiasis can cause an acute reactive encephalitis. Chronic or subacute meningitis due to tuberculosis or cryptococcosis, can occur in AIDS.

Worm infestations of the central nervous system tend to provoke severe symptoms. Infection with Angiostrongylus cantonensis, cysticerci, Echinococcus, Gnatostoma sp, Toxocara sp and ectopic migrations of schistosomes or Paragonimus sp usually cause acute symptoms. The cerebrospinal fluid can contain eosinophils. Schistosoma japonicum especially affects the brain during ectopic migration. S. haematobium and S. mansoni more often cause lesions in the spinal cord, though these findings are not proven.

Mefloquine -in some cases- causes severe side effects, such as confusion, dizziness or acute psychosis.

Individuals who take monoaminoxidase (MAO) inhibitors and experiment with plants that contain substances that can cause interactions with these (e.g. harmin contained in ayahuasca, Banisteropsis caapi) can develop acute confusion and delirium.

Cerebral oedema. In high mountainous areas one should watch out for acute cerebral oedema due to altitude sickness in cases of acute confusion, Cheyne-Stokes respiration, ataxia, disorientation or other neurological problems. Fast administration of oxygen and dexamethasone and immediate evacuation to an area at lower altitude with medical infrastructure is imperative. Acetazolamide (Diamox®) can be used prophylactically with limited efficacy.

It should of course be borne in mind that an already existing cardiovascular disease can worsen the relative hypoxia at high altitude.

A poorly burning stove in an unventilated environment can cause carbon monoxide poisoning (CO-intoxication).

Mefloquine taken for malaria prevention in low-lying areas and continued to be taken in the mountains can result in confusion. The same warning applies for alcohol.

Caisson disease. In acute confusion, stupor, neurological problems or shock occurring after diving, one should consider decompression problems or caisson disease resulting from too rapid ascent to the surface (often occurs in panic situations).

Rupture of the lung with pneumothorax can occur due to rapid ascent to the surface without adequate expiration. For example, the pressure amounts to 3 atmospheres at a depth of 20 metres while on the water surface it is only one atmosphere so that the lungs’ volume would have to increase threefold. The air in the lungs expands as the pressure falls.

Envenomation by certain marine animals can have hyperacute and very serious consequences. The sea wasp [Chironex fleckeri] is a small, translucent, but extremely venomous jellyfish that is found in Australasian seawater. Coneshells [Conus sp] can likewise deliver a highly venomous sting (nerve toxin). The bite of the so called “blue ringed octopus” [Hapalochlaena lunulata and H. maculosa], a name given to two related species of small cephalopods (15 cm) found in the seas between Northern Australia to Japan, is likewise notorious. Acute confusion and stupor are among the clinical symptoms. Irukandji syndrome occurs in North Australia following stings by Carukia barnesi, a small box jellyfish.

• Hypoglycaemia. Rapid recovery after administration of glucose. Check for any use or administration of antidiabetic medication and consumption of Akee fruit (syn. Ackee fruit, Blighia sapida; contains toxic hypoglycines A and B).

• Severe ketoacidosis, usually in diabetes

• Wernicke-Korsakoff’s disease (frequent with alcohol abuse). Acute deterioration can be triggered by intravenous glucose administration. Paresis of the eye muscles, together with ataxia in a patient with confusion and apathy, with recovery after injection of thiamine (vitamin B1), is diagnostic. (cf. beriberi)

• Severe hyponatraemia, such as is occasionally seen in SIADH (Syndrome of Inappropriate Secretion of Antidiuretic Hormone) and in Addisonian crisis (adrenal failure, e.g. after a bite from a Russell’s viper).

• Heat stroke and dehydration. Definitely increased risk in the tropics. Heat illness may be viewed as a continuum of illnesses relating to the body’s inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (ie, prickly heat), heat cramps, and tetany, as well as heat syncope and heat exhaustion. Heatstroke is the most severe form of the heat-related illnesses and is defined as a body temperature higher than 41°C associated with neurologic dysfunction. Two forms of heatstroke exist. Exertional heatstroke generally occurs in young individuals who engage in strenuous physical activity for a prolonged period of time in a hot environment. Classic nonexertional heatstroke more commonly affects sedentary elderly individuals, persons who are chronically ill, and very young persons. Classic nonexertional heatstroke occurs during environmental heat waves and is more common in areas that have not experienced a heat wave in many years. Both types of heatstroke are associated with a high morbidity and mortality, especially when therapy is delayed. Hypoglycemia, convulsions and rhabdomyolysis can occur as complications of heatstroke.

• Severe hypothyroidism with possible myxoedemic coma. Thyroid problems can get worse after using iodine for drink water decontamination.

• Drunkenness. Beware of methanol contamination of home-brewed liquors.

• Intoxication: acute e.g. CO, cocaine (crack), chronic in e.g. mercury- or thallium intoxication (rat poison). Intoxication with thallium causes hair loss several weeks after the acute poisoning.

• Epilepsy, post-ictal confusion. Neurocysticercosis is a major cause of epilepsy in large parts of Central and South America.

• Cerebrovascular accident due to thrombosis or cerebral embolism (increased risk in Chagas’ disease, endocarditis, sickle cell crisis).

• Loasis (Loa loa infection) with high microfilariaemia can cause acute neurological symptoms, often just after commencement of therapy.

• Hypertensive encephalopathy is usually clinically manifest. It is a medical emergency. Blood pressure is very high and the eye fundus is typical.

• Inflammation of the brain and/or meninges . Cerebral vasculitis can occur in a systemic disease such as systemic lupus erythematosus. Immunosuppression in SLE-patients, e.g. by therapy with steroids, increases the risk of some complications, such as tuberculosis, including meningeal tuberculosis (not infrequent in India). Beware of Strongyloides hyperinfection when people use corticosteroids.

• Head injury, with concussion or subdural haematoma.

Pathophysiology

• ED is essentially a vascular disease often associated with diabetes, hypertension, and CAD. Other conditions include neurologic disorders, endocrinopathies, BPH, and depression.

• Conditions associated with reduced nerve and endothelium function, such as aging, smoking, and hypercholesterolemia cause circulatory and structural changes in penile tissues, resulting in arterial insufficiency and defective smooth muscle relaxation. Sexual dysfunction may be the presenting symptom of these disorders.

• ED is often an adverse effect of many commonly prescribed medications such as psychotropic and antihypertensive agents.

Frequency

• In the Massachusetts Male Aging Study (MMAS), a community-based survey of men aged 40-70 years, 52% of the respondents reported some degree of erectile difficulty. Complete ED, defined as (1) the total inability to obtain or maintain an erection during sexual stimulation and (2) the absence of nocturnal erections, occurred in 10% of the respondents. Lesser degrees of mild and moderate ED occurred in 17% and 25% of responders, respectively.

• An estimated 18-30 million men in the US are affected by ED. Long-term predictions based on an aging population suggest a large increase in the number of men with ED.

Causes

• ED is divided into organic and psychogenic impotence, but most men with organic etiologies usually have an associated psychogenic component. Pure psychogenic ED is an uncommon disorder.

• Diabetes is a well-recognized risk factor, with approximately 50% of diabetic men experiencing ED.

• Cigarette smoking has been shown to be an independent risk factor, increased by a factor of 1.5

• A sedentary lifestyle is a contributing factor to ED. Exercise has a beneficial effect on the cardiovascular system, and men who exercise regularly have a lower risk of ED.

• Vascular diseases account for nearly half of all cases of ED in men older than 50 years. Vascular diseases include atherosclerosis, peripheral vascular disease, myocardial infarction, and HTN.

Medication	Advantages	Disadvantages
Hormonal (testosterone) therapy	May restore sexual desire Patches now available	Useful only in the few patients with abnormal hormone levels Significant adverse effects (eg, fluid retention, liver damage) Limited effectiveness
Vasodilators (nitroglycerine)	Painless May use treatment only when desired	No reports on long-term use Possibly common adverse effects (eg, headaches) Very high failure rate Very limited effectiveness
Yohimbine (Yocon)	Adverse effects uncommon May increase sexual desire Success rate of 20-25%	Need to take medication every day No reports on long-term use Adverse effects, including nervousness, headache, dizziness, and nausea Limited effectiveness
Pentoxifylline (Trental)	Adverse effects uncommon Success rate of 50%	Adverse effects, including headache, dizziness, and stomach upset May only help with marginal penile blood
Trazodone (Desyrel)	Adverse effects uncommon Estimated success rate of 25%	No reports proving benefit No reports on long-term use Adverse effects, including lethargy and drowsiness Limited effectiveness
Intraurethral pellet therapy (MUSE)	May use treatment only when desired Success rate of 45% Reasonably effective	Pellet must be inserted directly into penis through urethra Requires refrigeration Mild burning or discomfort experienced by 30% of patients Can cause mild dizziness, faintness, or low blood pressure

• In vasodepressor syncope, there is peripheral vasodilation to increase blood flow to the muscles, leading to blood pooling and a decrease in venous return and heart rate. This causes syncope.

• When dealing with seizure disorders, it’s very important to get a good family history. There’s not always an obvious inheritance pattern with genetic epilepsies, so it’s often helpful to get a history from the grandparents of the patients if possible as well.

• Blocking voltage dependent sodium channels at high firing frequencies is an effective way to block seizures since this interferes with “bursting” neurons, which are the likely drivers of epilepsy.
  

Neuromuscular problems can be isolated to the motor neuron, peripheral nerve, neuromuscular junction and the muscle itself.

Pathological processes can attack the myelin surrounding the nerve (think immuno-mediated) or the axon itself.

	Disease	Distinctive Clinical and Pathological Features	Etiology
Anterior Horn Cells	Amyotrophic Lateral Sclerosis	Only disease with muscle wasting and increased reflexes Specifically targets large motor neurons and corticospinal neurons	Appears to be due to a toxic gain in function of superoxide dismutase
	Spinal Muscular Atrophy	Does not affect mental faculties (as opposed to DMD) If children can survive childhood, they often live a normal lifespan	Due to degeneration of motor neurons in spinal cord Assoc. w/defect of SMN1 gene on 5q
Plexuses	Brachial Neuritis	the sudden onset of severe pain, usually about the shoulder and often beginning at night, leading to a “flailed arm” in a week or two no Tx; usually resolves spont.	Autoimmune process-- often preceded by an upper respiratory infection, hospitalization, vaccination, or non-specific trauma
		Brachial plexus is also susceptible to infiltration by lung/breast CA; assoc. w/ tremendous pain
Involving the Peripheral Nerves	Hereditary aka Charcot Marie Tooth	It usually involves the legs before the arms Can be mild and slowly progressive, so w/o patients w/high arch problems (“marked wasting of the more distal extremities, particularly the peroneal muscle groups, resulting in ‘stork legs.’”) If a patient loses all peripheral sensory fibers, they often develop a mutilating neuropathy and present w/ cuts, burns, etc. on their hands.	PMP 22 gene duplication assoc. w/autosomal dominant type
	Diabetic neuropathy	Effects mostly feet, hands Pain predominates over weakness
	Vasculitic neuropathy	Differential fasicular loss is the hallmark of vascular process affecting the peripheral nerves
	Guillian Barre syndrome	Attacks peripheral myelin (as opposed to central in MS) but anywhere along its course, so patients can present w/ proximal or distal weakness Classic presentation is profound weakness and early loss of reflexes Can lead to severe weakness and even death	Inflammatory cells attack myelin; esp. post-Campylobacter infection antibodies attacking motor neurons Most often a mixed neuropathy w/some sensory loss

In muscle diseases, largest and most proximal muscles (gluteus, shoulders, hips) are usually affected first and most severely.

When evaluating patients with muscle weakness…

If muscles appear to be normal sized acquired muscle disease

If muscles appear wasted dystrophy

Lordotic sign = combined backward and lateral curvature of the spine, “hip dips on stepping up”

Class		Clinical Presentation	Etiology	Treatment
Autoimmune	Progressive muscle weakness w/ or w/o pain CK elevated in active stage, and it is the most useful test for dx; CSR less helpful		Derm.: via circulating Ab’s Poly.: involves T4 lymphocytes Derm./Poly.: assoc. w/ autoimmune diseases	Modulate immune system
	Inclusion body myositis: insidious, slow, painless		Biopsy shows inflammation and inclusions	Does not respond to immune modulation
Toxic	Colchicinemicrotubule damage
	AZTmitochondrial toxicity
	Steroids: if you give steroids to patients w/ myositis, be sure to distinguish primary sxs from side effects
Metabolic	Acid maltase: in infants, see muscle weakness, organomegaly (esp. tongue), cardiac involvement & death w/in a few mo.s
	McCardle’s disease: muscle pain post exercise w/rhabdomyolysis increased CK
	Critical illness myopathy: GI infection Txed w/ corticosteroidspatient now on ventilator and can’t wean off; dev. myosin deficiency			Takes mo.s to clear; Tx is supportive
Endocrine	Hypothyroidism: elevated CK & muscle inflammation Hyperthyroidism: strabismus		Give all people w/ muscle disease a thyroid test
Hereditary	DMD: pseudohypertrophic calves, fibrosis and fat make muscles look bigger 75% have intellectual impairment CK in the 1000s Can usually talk and swallow until late in the course
	FSH: scapula rises when you raise arms; no wrinkles on forehead

• Nerve Transmission – nerve action potential moves along a terminal; voltage-gated Ca channels open; vesicles exoctyose at specific active release zones; Ach is released and binds to the post-synaptic membrane to make an action potential => if large enough, muscle fiber AP; Ach hydrolyzed by AchE with choline reuptake.

• 300 000 main store of Ach; 10 000 mobilization Ach; 1000 releasable Ach.

• Small depolaraizations are called MEPPs (mini end plate potentials)

• EPP must reach the AP threshold to generate an AP (safety factor guarantees muscle activation).

• Disorders may be divided into pre-synaptic, post-synaptic based on the compound muscle action potential (CMAP):

Diseases	Single shock	Slow rate	Fast Rate
MG (post)	Normal	decrements	decrements
LEMS (pre)	small	decrements	increment
Botulism (pre)	small	decrements	increment

There are two mechanisms for the slow rate decrementation seen in both pre and post-synaptic disorders (see Syllabus for individual description and variability). For fast rate, build-up of Ca helps presynaptic but does not affect the post-synaptic because too few receptors.

MG – clinical picture characterized by intermittency of weakness and ocular changes, overt progressive weakness that is alleviated by rest (eyes closed shut for a while are better, but may progressively worsen). Symptoms may be worse in the evening, worse in cold weather situations. The differential often includes MS which can be separated by CNS involvement.

• MG tested by edrophonium, treated with neostigmine or pyridostigmine (AChE inhibitors)

• The post-synaptic muscle membrane is altered by anti-Ach receptor antibodies, making the membrane less sensitive to applied Ach. There are reduced numbers of quanta released as a result => small EPP, below threshold. Reduced probability that a nerve potential will be followed by a muscle action potential.

• Electromyography of MG patients reveals that the CMAP of nerve stimulation is normal. The amplitude of the 4th or 5th nerve stimuli falls to 10% of the initial value. Unfortunately, repetitive nerve stimulation is not a sensitive test for MG dx.

• Single fiber EMG shows jitter in some muscles in almost all patients with MG. Jitter is not specific, but a general sign of disturbed neuromuscular transmission. Jitter is useful in excluding abnormal neuromuscular transmission (ie jitter in a weak muscle puts NM transmission problems low on the differential). Jitter is the most sensitive in vivo test of NM transmission.

Botulism – clinical picture characterized by rapid onset with descending weakness (cf to G-B which is an ascending disorder), blurred vision, dysphagia, dysarthria, dry mouth & other reverse SLUDS. Think food (not properly cooked, nearly endemic in some Alaskan villages), wounds, cocaine use, colostomy bag contamination. Presentation among children is a hypotonic kid with a poor suck who recently ate some honey from PA, CA (clostridium botulinum). Kids have a better chance of isolating bug in poo.

• Botulinum toxin is one of the most deadly known to man, and destroys the neurotransmitter pre-synaptically.

• Botulinum toxin used to treat achalasia (remember from GI?), cervical dystonia, and blink spasms.

1. Primary HIV diseases – encephalopathy, neuropathy

2. 2^nd infections – toxo, crypto, PML

3. ART effects on neurological fxn.

PRIMARY DISEASES OF HIV

• Pirmary HIV encephalopathy – may or may not be clinically picked up during the initial HIV infection (often recalled within a hx of HIV) – headache +/- meningismus, may be mistaken for Mono. Usually encephalopathy clears, but may not in some patients, instead progressing and rarely being fatal.

• HIV encephalopathy aka AIDS Dementia Complex aka Late-Stage HIV encephalopathy –encephalopathic picture unique to HIV patients, now limited by HART to under 5% of HIV pts. Progressive memory and other problems, extreme apathy and indifference (not depressed) – may take a patient 30 seconds to respond to a simple question. Clinical assn. with myelopathy. Must rule out 2^nd infection and tumor.

• MRI reveals hydrocephalus ex vacuo (brain shrinkage). Use of PCR to rule out viral infection.

• Outlook much better post-HART.

• HIV does not enter but destroys neurons. HIV infects the macrophages that cross the BBB (Trojan horse); activate astrocytes to make toxic cytokines and generate an inflammatory response.

• Best tx involves keeping the CD4 counts as low as possible.

• HIV peripheral neuropathy – occurs in approximately 30% of all AIDS patients. May be clinically identical to G-B, necessitating HIV test in any presentation of G-B with any HIV risk factors. This demyelinating disease is the result of a disrupted immune system, with antibody and cytokine mediated nerve damage. Increased incidence of Bell’s palsy.

  • Tx includes steroids, plasma exchange, IV IG – usually self-limiting (months to years).

SECONDARY INFECTIONS

• Toxo, Crypto, PML are all covered well in the notes.

DRUGS

• Nucleoside analogs like ddI, ddC, or d4T may cause foot pain, serious toe pain secondary to the meds. Drug-induced neuropathies need to be realized soon because they can be made chronic if the drug is continued. Sometimes HIV pts need these drugs, and you are balancing the need for low CD4 count with the neuropathy induced by nucleoside analogs. Soft ground.

• Thalidomide and dapsone are AIDS-related meds that may cause neuropathy.

• Movement disorders were well-covered in the syllabus, and only the fun video will be covered below:

• PD – resting tremor, bradykinesia, drooling, shuffling gait, difficulty turning, script is legible but small, pill-rolling “resting” or Parkinsonian tremor, difficulty rising from a chair.

• Progressive supranuclear palsy – similar to PD; loss of eye mobility, gait problems, pseudobulbar palsy.

• Shy-Drager Syndrome – impotence in men, orthostatic hypotension in women, also autonomic insufficiency.

• BET – benign essential tremor – assn. with activity, absent at rest, faster than PD (7-8 Hz vs. 4-5 Hz for PD), no PD, 50% have a family history. Also called senile tremor, also called familial tremor, also called action tremor.

• Lhemitte’s sign: unknown maneuver that results in stretching of axons and pain.
• 
  
• Marchiafava-Bignami syndrome: results from EtOH consumption, esp. red wine.
• 
  
• Binswanger’s: lots of ministrokes, .
• 
  
• Marcus Gunn pupil aka swinging flashlight test = bad eye doesn’t provide consensual constriction.
• 
  
• Internuclear ophthalmoplegia: dis coordination of lateral gaze.
• 
  
• Dysmetria: movements that aren’t fluid.

One of the major things of the neurological exam is to be aware of the subdivisions. If someone comes into you as a new patient, CCHR, PIM, components of the exam that are relative to the history and also when you come to your review of systems. If you have the list in front of you, you are less likely to omit an exam.

Divisions:

• Mentation and Speech

• Cranial Nerves- most neurologists don’t do cranial nerve one.

• Motor- with several subdivisions. usually is the most important and the most robust. So when you are involved with patients that are lathergic or noncompliant or can’t cooperate it can give you important information/ good results when other divisions do not.

• Reflexes- lot of them in the book.

• Cerebellar- good coordination is dependent on good strength. Poor control versus poor cerebellar function

• Central Exam- more subject to a variety of error, be aware of the component

• Meningial Irritation- just keep in mind this is a part of the examination

How do you differentiate Cerebellar problems from those of the 8^th CN?

Presence or absence of Nystagmus (vestibular system problem when nystagmus is present) 90% seperation

Mentation- diagnosing the mental status

1. Level of consciousness. Descrease level on conciousness affects everyting else. Comatose- very little that you can do. You can grade them on a Glaslo carma (?) scale or just a description of how well they react. Do you have to arouse them? How much response do you get? Intellectual impairment and dementia diagnosis are also an element of the mental status- Alzheimer’s. To evaluate the intellectual function Minimetal status exam- came in 1974, many people use it worldwide- formalized to say what you do and don’t do. In terms of the evaluating the intellectual function, we find the information very important. A health brain in the US knows the president and the mayor, maybe the vice president- all important components of the healthy fund of information. Loss off long-term memory is involved in the fund of information (name, hometown)- in general more hard wired in. When diseases set in, these things will stay more then other things. Remote fund of information- its components are very wide.

2. Digit Span Random digit- immediate recall. Give the patient a string of 7 number and have them say it back to them. The average person can usually remember 7 digit in a span. One of the many things in the examination that are anxiety sensitive. Anxiety- non anxious patients will do better then those that are anxious. Many things are also culturally dependent (prior exposure needed)- ex. president of US. Someone in another culture may not know this. Usually you do a battery of tests.

3. Recent Memory- tell them a group of number or names and then come back in two minutes and ask you what those were. Requires you to remember store and recall information. More reliable then the immediate memory or the remote memory. For each test and the entire examination, you need practice and some grasp of the normal.

4. Orientation- for person, place and time- ex. what’s your name? some people call that orientation to person (adequate), or ask him what is it that I do- doctor, professor. What is the name of this place?- Howard University. Time is less stabile.

Speech

The biggest part is to know if the person has any phagia, and/or any significant dysfunction. Usually you can just talk to the person and you actually know if they have normal speech. What are the components of speech that you should be aware of:

1. Ability of a patient to follow commands. First order (open your eyes, raise your hand) monitors comprehension. #1 parameter concerning prognosis and communication. If the comprehension survives then it is a better prognosis (brain damage)

2. Speech production- do they produce loud volume of speech, is it fluent, or is it broken. Look for a lot of hesitation. Disturbance in speech flow is associated Broca’s Area- anterior aphagia Reduction in speech flow, fluency and amount produced. In the Broca’s aphagia, temporal and parietal lobes involved, but among the problems is with comprehension.

3. Naming

4. Repetition- Mary had a little lamb, count to 10.

You should also have the patient read and write. Core of speech evaluation

Motor Examination

1. Strength- Observe the patient. If you have a patient with a hemiplegia then you should look to see how much they move on the left and then on the right. The same with a hemiperesis. Look for differential movement. Tell the patient to do something, close the eyes and hold out hand. Weak arm will drop down. Compared one side to the other (left and right biceps)-very important. Test deltoid and dorsal wrist flexion (proximal vs. distal strength also). Hip flexors, knee extensor. Write it down based on which joint is doing what. When you test the individual muscles you want to see if there was weakness, (direction). Ex. there was weakness in the lower limbs, but not in the upper limbs (paraparesis), weakness on the left side but not on the right side (left-sided hemiparesis), proximal weakness but not distally (muscle dysfunction). Peripheral neuropathy- weakness distally but nor proximally

2. Tone- passive range of movement, look for equal resistance in either direction or any resistance. Increased tone with UMN lesions and basal ganglia disorders. Exam elbows, knees and wrists. Decreased tone with LMN lesions

3. Inspection- Look for wasting, differential, proximal or distal LMN lesion. Fasciculation LMN lesion

Tell patient to elevate the limbs, weaker side won’t go as high. Test them against resistance.

Walk the patient to determine the gait, very important. (cerebellum examination) If you do not walk a patient then your examination is incomplete.

Reflexes

Always want to compare R and L, upper and lower, proximal and distal. Biceps jerk, tricep jerk, knee jerk, ankle jerk, and the superficial reflexes (abdominal and cremasteric). Babinski reflux (normally the big toe will go down)- upper motor neuron lesion. But some may not have the sign.

No ankle jerk LMN lesions, clinically, peripheral neuropathies- worse in lower limbs then in the upper limb. Slipped disk  loss of ankle jerk (was very important)

Cerebellum

• You want them to tandom walk, one foot in front of the other. If you can’t walk the patient, you can’t say the cerebellum is normal. Tandom walking requires more cerebellar involvement. It is the more demanding task that uses the cerebellum in the lower limb.

• Heel-shin test- some people can’t dorsal flex so they can’t give you full cooperation.

• Alcoholic Cerebellum Degeneration (perenkymal cerebellum degeneration)- alcohol has short term effects on the cerebellum. Heavy drinking and malnutrition combined give you the ACD- long term and chronic ( Audio was bad at this point)

• Upper limb finger nose test- past pointing, intentional tremor, overshooting. You have to practice, especially on people with pathology.

• Other test of the cerebellum influenced by strength and can be misleading. So if you have you strength intact you can overcome some of the cerebellar problems.

• Normal cerebellum and muscle weakness on the left non-coordination

Sensory Test- many parameters

Pain and Temperature

HIV- pain was done with a pin, but it is done far less now because of AIDS and HIV. It is still a valuable parameter. They should tell you if it is sharp or dull, compare right with left in the face and the limbs. Compare the upper limbs with the lower limbs- to see if you have a spinal cord lesion leading to paraparesis. Can you feel it proximally or distally? Proximal will be better then distal in different neuropathies (ex. diabetic neuropathy). Wood pin is not as reliable as the safety pin.

Temperature- tested less often. The way around it is to use the tuning fork and ask them if the metal feels cold. Make sue to measure, proximal vs. distal, etc. Pain and temperature is carried in the Spinothalamic tract (tells you about the lateral column). Joint position test- Take the finger and tell if it is up or down. Can tell you if there is a proprioception problem

Romberg sign- people argue about it in the literature. Can you stand with your feet together and your eyes closed, need good proprioception and a good cerebellar system. Many people with cerebellar system dysfunctions tend to separate their heels. Small amount of triangle makes it a better base.

Vibration/Tuning forks- compare right with left, upper and lower, and compare the proximal and distal. Relatively subjective- a lot depends on how hard you strike the tuning fork. Hitting it hard can give them a very forceful sensation that they can pick up. You should be able to just detect it in their fingers- objective only if you (as the normal) can only feel it in your fingers.

Signs of Meningial Irritation- relatively simple, (couldn’t understand what he was saying) get the patient to relax- when you flex the neck reflex flexion of the patient’s head Brazinski sign. Nextitin (?)

Curinate sign- Flex the hip and attempt to extend the knee (normal person should be able to completely extend the knee). Meningial irritation limited extention or pain in the proximal thigh. Meningial irritation is found in meningitis (bacterial, viral, chronic, and subacute) and with subarachnoid hemorrhage (aneurysm ruptures).

Cranial Nerves

CN2- visual pathway- need to be aware of it. Visual acuity- Rosenbaum chart, should be 14 inches away from the face with bright light. 20/200-legally blind, 20/20 is considered normal. Highest on the chart is 20/800. Should do each eye separately. Confrontation of visual field. Should test each eye separately. Each eye has four quadrants and you should be able to demonstarate vision in each field. Small stationary is more useful the a large moving object.

Right hemiparesis- can be caused by a lesion in left internal capsule lesion. Damage of fibers going to the left occipital cortex- cover vision from the right side of the face and started from the left side of the retina. They will also have a right-homonomous hemianopsia. Most common visual problem. Quadrantanopsia is also a problem.

Bitemporal hemianopsia associated with pituitary adenoma. Damage to the medial fibers in the optic chiasm, dealing with vision from the temporal field.

Papillary Light reflex- CN2 and CN3. Both pupils should constrict when light is shined into one eye- consensual and direct light reflex. Should look at the charts and you should be able to determine the size of the pupil (need to write down how big the pupil was and if both pupils responded to light), may want to look at accommodation.

CN3, CN4, CN6- all concerned with eye movements. You can test the eyes separate or togther, but you have to test for conjugate gaze. Lateral and Medical Rectus- horizontal gaze. Look to right and up- superior rectus. To the right and down- infereior rectus. Medially and up- superior oblique. Medially and down- inferior oblique

Is there conjugate gaze? If they are not, then which muscle is it?

Double vision- diploplia. Double vision only on lateral gaze (left lateral or left medial rectus is not performing properly). Nystagmus- says that something is probably a problem in the vetibular system.

CN7- Moves the facial musculature (is the smile line different on each side), taste to anterior 2/3 of the tongue. Can not open the eyes or raise the eyebrows if there is a problem. If the eye is widely open CN7 problem/weakness (Audio was bad here)

CN8- observe for nystagmus- very valuable, tells you there is vestibular dysfunction. Auditory acuity on one side versus the other. Ask the patient what they hear with their eyes closed. Weber test- put tuning fork in the middle of the forehead. Rienne (sp?)test, put tuning fort on the mastoid process and then put it at the external ear and ask the patient which one is louder. Air conduction is usually louder.

CN 9, CN10, CN11, CN12-

CN12- innervates the tongue. The tongue deviates if one side is weak. Deviates towards the affected side of the tongue.

Fasiculations of the tongue- LMN lesion associated with hematotrophic lateral sclerosis

Corticobulbar lesion will give you a contralateral sign. Lower Motor Neuron lesion will give you an ipsilateral sign.

Here are some of the clinical signs that are seen in meningitis. Some of them are quite common, however, some of them are quite rare...

1)Neck rigidity:

It is resistance to passive flexion of head, an early sign of meningitis..
It is d/t spasm of extensor muscles of neck..
It can be tested by asking pt to place chin upon chest, which can not be done...

2)Kernig's sign:

With pt's hip flexed, the examiner tries to extend the knee as far as possible. Normally the knee can be extended so that the angle b/w posterior surface of thigh & leg is about 135 degrees.
In positive Kernig's sign, the angle is less d/t spasm of hamstring muscles & pain arises as a result of stretching of the spinal nerve-roots of the lower limb, the lower end of the subarachnoid space of the spinal cord being distended & spinal meninges inflamed...

3)Brudzinski's signs:

a) Neck sign: Flexion of the hips & knees on flexing the neck or turning it to one side..

b) Leg sign: On flexion of one lower extremity, there is automatic flexion of the opposite lower limb..

c) Pubic sign: Flexion of both knees on pressure over symphysis pubis..

d) Chick sign: Flexion at both elbows on pressure over chick bones..

4)Lasegue's sign:

With pt lying on back & both legs fully extended at knee, the examiner passively flexes each leg at hip while keeping the knee joint extended. Normally the straight leg can be lifted to an angle(with horizontal) of 65 to 90 degrees.
In case of meningitis, this angle is reducud & pain & limitation of movements present earlier.

5)Gullian's sign:

On applying pressure or pinching over one quadriceps muscle, there is flexion of contralateral hip & knee..

6)Leichtenstern's sign:

On gentle tapping of bones of extremities, there is pain & patient may wince, draw back suddenly or cry out loudly..

7)Signorelli's sign:

There is extreme tenderness on palpation of retromandibular joint..

8)Simon's sign:

It is seen early in meningitis..
There is in-coordination of movements of the diaphragm & the thorax..

9)Bikele's sign:

With patient holding arms abducted & forearms flexed, examiner tries to extend the forearms. This is quite painful & can not be done easily in meningitis..

Seen in Neuroblastoma..

PeppeR- Right Side - liver metastasis

Hutchinson - Left Side orbital metastasis

Skin - Blue Berry Muffin Syndrome