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General Examination Proforma (Neurology Focused & Structured)

I. BioData (Identification Data)

  • Name:

  • Age/Sex:

  • Occupation:

  • Education:

  • Informant:

  • Date of Examination:

  • Presenting Complaints and history:

GENERAL EXAMINATION

II. Level of Consciousness and Orientation

  • Level of Consciousness:

    • (Alert, Lethargic, Obtunded, Stuporous, Comatose)

    • If altered, document Glasgow Coma Scale (GCS) score:

      • Eye Opening (E):

      • Verbal Response (V):

      • Motor Response (M):

      • Total GCS:

  • Orientation:

    • Time: (Oriented / Disoriented)

    • Place: (Oriented / Disoriented)

    • Person: (Oriented / Disoriented)

  • Cooperation & Attitude: (Cooperative/Uncooperative, agitated, restless, withdrawn)

  • Speech (General Observation): (Normal flow, volume, articulation, presence of dysarthria, aphasia, dysphonia)

III. Built and Nourishment along with BMI

  • Built: (Lean / Average / Obese / Asthenic / Pyknic)

  • Nourishment: (Well-nourished / Undernourished / Cachexic) – Note any disproportionate muscle wasting.

  • BMI (Body Mass Index):

    • Weight (kg):

    • Height (m):

    • BMI = Weight (kg) / [Height (m)]²

    • (Underweight <18.5, Normal 18.5-24.9, Overweight 25-29.9, Obese ≥30)

IV. Pallor, Icterus, Cyanosis, Clubbing, Lymphadenopathy, Edema

  • Pallor: (Present / Absent) – Examine conjunctiva, nail beds, tongue.

  • Icterus: (Present / Absent) – Examine sclera, skin.

  • Cyanosis: (Present / Absent) –

    • Central: (Tongue, lips) – Sign of hypoxemia, consider respiratory failure affecting brain.

    • Peripheral: (Nail beds, extremities).

  • Clubbing: (Present / Absent / Grading) – (Typically not directly neurological, but associated with systemic conditions).

  • Lymphadenopathy: (Present / Absent) –

    • Location: (Cervical, axillary, inguinal, supraclavicular, etc.)

    • Size, Consistency, Tenderness: (e.g., firm, matted, rubbery, tender).

    • (Relevant if underlying systemic infection or malignancy has neurological manifestations).

  • Edema: (Present / Absent) –

    • Location: (Pedal, sacral, periorbital, generalized)

    • Type: (Pitting / Non-pitting)

    • (Primarily systemic causes, but chronic immobility in neurological conditions can contribute).

V. Neurocutaneous Markers

  • Skin:

    • Café-au-lait spots: (Number, size, distribution) – Neurofibromatosis type 1.

    • Neurofibromas: (Cutaneous, plexiform) – Neurofibromatosis type 1.

    • Ash-leaf spots: (Hypopigmented macules, best seen under Wood's lamp) – Tuberous Sclerosis.

    • Shagreen patches: (Pebbly, raised skin lesions, typically over sacrum) – Tuberous Sclerosis.

    • Facial Angiofibromas: (Reddish papules on face) – Tuberous Sclerosis.

    • Port-wine stain (Nevus flammeus): (Unilateral facial, follows trigeminal distribution) – Sturge-Weber syndrome.

    • Telangiectasias: (Conjunctival, ear lobes) – Ataxia-telangiectasia.

    • Any other unusual skin lesions, rashes, or scars:

VI. Signs of Craniovertebral Junction (CVJ) Anomalies

  • Neck Inspection: (Short neck, webbed neck, low hairline – e.g., Klippel-Feil syndrome).

  • Spine Palpation: (Tenderness, steps/gaps, especially over cervical spine).

  • Neck Movements: (Range of motion – flexion, extension, rotation, lateral flexion; presence of pain or crepitus).

  • Head Posture: (Any abnormal tilt or sustained posture).

  • Neurological Deficits: (Look for long tract signs, lower cranial nerve palsies – these are direct neurological examination findings but often associated with CVJ issues).

VII. Signs of Inherited Peripheral Neuropathies

  • Muscle Wasting: (Distal muscle wasting, e.g., 'inverted champagne bottle' legs in Charcot-Marie-Tooth disease).

  • Foot Deformities: (Pes cavus, hammer toes) – Classical for CMT.

  • Hand Deformities: (Claw hand, muscle wasting in intrinsic hand muscles).

  • Motor Weakness: (Distal weakness, foot drop – detailed motor examination follows general exam).

  • Palpable Nerves: (Thickened peripheral nerves, e.g., ulnar, greater auricular, peroneal nerves – in some demyelinating neuropathies like HNPP, leprosy).

VIII. Signs of Inherited Ataxias

  • Gait: (Ataxic, broad-based, reeling, staggering – observe if patient is ambulating).

  • Dysarthria: (Slurred, scanning speech).

  • Nystagmus: (Involuntary eye movements, especially gaze-evoked).

  • Scoliosis/Spinal Deformities: (e.g., Friedreich's ataxia).

  • Foot Deformities: (Pes cavus – common in Friedreich's ataxia).

  • Cardiac Signs: (Cardiomyopathy – e.g., Friedreich's ataxia).

  • Ocular Motor Abnormalities: (Slow saccades, ophthalmoplegia – e.g., spinocerebellar ataxias).

  • Any other involuntary movements or coordination deficits.

IX. Vital Signs

  • Pulse: (Rate / min, Rhythm, Volume, Character, Condition of vessel wall).

  • Blood Pressure: (Systolic / Diastolic) – Record in right upper limb in sitting position. (If indicated, assess for postural drop by recording in supine and standing positions).

  • Respiratory Rate: (Breaths / min, Rhythm, Type of respiration – Thoracoabdominal, Abdominal, Predominantly Thoracic).

  • Temperature: (°F / °C) – (Oral/Axillary/Rectal).

  • SpO₂: (Oxygen saturation, room air or with O₂ support).


Viva Questions and Answers on General Examination (Neurology Focused)

Q1: "You've systematically documented the patient's level of consciousness using GCS. Can you briefly explain what GCS assesses and its utility in general medicine, not just in neurology?"

A1: "The Glasgow Coma Scale (GCS) is a standardized tool used to assess a person's level of consciousness based on three components: eye opening, verbal response, and motor response. Each component is scored, and the sum gives a total score out of 15. Its utility in general medicine is profound because it provides an objective, repeatable measure of neurological status. It helps in:

  1. Detecting deterioration: Any drop in GCS score warrants immediate attention.

  2. Prognostication: A lower GCS often correlates with a poorer prognosis in various conditions.

  3. Guiding management: For instance, intubation criteria might be based on a GCS of 8 or less.

  4. Communication: It provides a common language for healthcare professionals across specialties."

Q2: "Why is assessing a patient's posture and gait important during a general examination, even before a detailed neurological assessment?"

A2: "Observing posture and gait in the general examination provides crucial initial clues to underlying neurological or musculoskeletal pathology. Abnormal postures like a 'parkinsonian stoop,' 'hemiplegic gait,' or 'foot drop' become immediately apparent. A broad-based ataxic gait, for example, can suggest cerebellar dysfunction, while a scissoring gait points towards spasticity. These early observations guide the subsequent focused neurological examination, helping to identify the system involved and often the broad anatomical localization of the lesion."

Q3: "You've specifically listed Neurocutaneous Markers. Why are these so important in a general examination for neurological cases?"

A3: "Neurocutaneous markers are vital as they are external manifestations of underlying neurological disorders, often genetic, known as neurocutaneous syndromes. Finding a single café-au-lait spot or an ash-leaf spot on general examination can point towards significant conditions like Neurofibromatosis or Tuberous Sclerosis, which can have diverse neurological implications such as seizures, cognitive impairment, brain tumors, or strokes. Their presence, or absence, helps guide further investigations and management, sometimes even suggesting a diagnosis without extensive invasive tests."

Q4: "Regarding signs of Craniovertebral Junction (CVJ) anomalies, what specific findings would make you suspect a CVJ anomaly on general examination, and why is early detection critical?"

A4: "On general examination, suspicion of CVJ anomalies would arise from observations like a short neck, webbed neck (Klippel-Feil syndrome), or a low hairline. Palpation might reveal tenderness over the cervical spine or a step deformity. Restricted neck movements or an abnormal head posture (like torticollis) could also be clues. Early detection is critical because CVJ anomalies can cause progressive neurological deficits due to compression of the brainstem, cerebellum, or spinal cord. These can lead to spasticity, lower cranial nerve palsies, gait disturbances, and even sudden death. Prompt diagnosis allows for potential surgical correction or management to prevent irreversible neurological damage."

Q5: "In the context of inherited peripheral neuropathies, you mentioned looking for 'pes cavus' and 'hammer toes'. What is the significance of these foot deformities?"

A5: "Pes cavus (high arched foot) and hammer toes are common and often early physical stigmata of chronic peripheral neuropathies, particularly those with a genetic basis like Charcot-Marie-Tooth (CMT) disease. They result from chronic muscle imbalance and weakness in the foot muscles. Their presence on general examination immediately raises suspicion of an underlying inherited peripheral neuropathy, guiding the examiner to look for other signs like distal muscle wasting ('inverted champagne bottle' legs), absent deep tendon reflexes, and sensory loss, even before detailed neurological examination."

Q6: "You mentioned observing for dysarthria in the general survey. How can you differentiate between different types of dysarthria just by general observation, and what might each imply?"

A6: "While formal assessment comes later, initial general observation can give clues:

  • Spastic dysarthria (UMN lesion): Strained-strangled, harsh, monotonous, slow speech (e.g., in pseudobulbar palsy).

  • Flaccid dysarthria (LMN lesion): Breathy, nasal, imprecise consonants (e.g., in bulbar palsy).

  • Ataxic dysarthria (Cerebellar lesion): Drunken, scanning (separated syllables), irregular rhythm (e.g., in cerebellar ataxia).

  • Hypokinetic dysarthria (Parkinsonism): Monotonous, quiet, rapid, mumbled, often festinating.

  • Hyperkinetic dysarthria (Chorea/Dystonia): Irregular articulatory breakdowns, sudden changes in pitch/loudness.